PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11205704-3 2001 The renin-aldosterone system is a major determinant of sodium balance in pregnancy. Sodium 55-61 renin Homo sapiens 4-9 11211621-0 2001 Influence of sodium intake on the reliability of active renin as a measure of the renin-angiotensin system in essential hypertension. Sodium 13-19 renin Homo sapiens 56-61 11460589-14 2001 The genes coding for components of renin-angiotensin system have drawn special attention, due to the central role that this system plays in the regulation of blood pressure, sodium metabolism, and renal hemodynamics. Sodium 174-180 renin Homo sapiens 35-40 11327100-3 2001 It now appears clear that a central feature of obesity-associated hypertension is related to changes in sodium handling that may result from abnormalities in sympathetic nervous system activity, the renin-angiotensin-aldosterone system, natriuretic peptides, and kidney function. Sodium 104-110 renin Homo sapiens 199-204 11116129-9 2000 The responses to central administration of angiotensin II-type AT(1)-receptor antagonists into the ventricular system or microinjected into the rostral ventrolateral medulla are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 renin Homo sapiens 218-223 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 95-101 renin Homo sapiens 52-57 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 95-101 renin Homo sapiens 155-160 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 202-208 renin Homo sapiens 155-160 11061347-3 2000 In short-term clinical studies, very low sodium intake (<50 mmol/d) has been associated with greater values for total and low-density lipoprotein cholesterol, fasting and post-glucose insulin, uric acid, plasminogen activator inhibitor-1, and activity of the renin-angiotensin system. Sodium 41-47 renin Homo sapiens 262-267 11082152-3 2000 To make that comparison, we studied healthy volunteers in balance on a 10-mmol sodium intake to activate the renin system. Sodium 79-85 renin Homo sapiens 109-114 11078175-11 2000 In patients taking amlodipine, the fall in plasma renin ameliorates the effect of sodium retention on BP. Sodium 82-88 renin Homo sapiens 50-55 11213538-3 2000 The second part reviews the four factors frequently cited as possible causes for this sodium retention: insulin resistance, alteration in the renin-angiotensin system, altered vascular responsiveness and alterations in the sympathetic nervous system. Sodium 86-92 renin Homo sapiens 142-147 10999820-2 2000 Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. Sodium 50-56 renin Homo sapiens 0-5 10894022-5 2000 The renal sodium retention in congestive heart failure is a consequence of the activation of the sympathetic nervous system and of the renin-angiotensin-aldosterone system. Sodium 10-16 renin Homo sapiens 135-140 11881033-1 2000 We have documented, contrary to expectation, that the renin-angiotensin-aldosterone system (RAAS) is stimulated normally by restriction of sodium intake inpatients with Type 2 diabetes mellitus (DM) and hypertension. Sodium 139-145 renin Homo sapiens 54-59 11174896-1 2000 Low-renin hypertension is common and usually implies increased retention of sodium (Na(+)). Sodium 76-82 renin Homo sapiens 4-9 11048827-4 2000 CONCLUSIONS: The lower resistance indices of the uterine artery during sodium restriction might reflect an increase in pulse pressure/impedance ratio as a result of activation of the renin-angiotensin system. Sodium 71-77 renin Homo sapiens 183-188 11049696-1 2000 INTRODUCTION: Dietary sodium restriction results in activation of the renin-angiotensin-aldosterone-system. Sodium 22-28 renin Homo sapiens 70-75 11049696-2 2000 In the non-pregnant situation renin release in response to a low sodium diet is mediated by prostaglandins. Sodium 65-71 renin Homo sapiens 30-35 10954007-1 2000 BACKGROUND: Additive hemodynamic effects of combined blockade of the renin-angiotensin system by an angiotensin I converting enzyme inhibitor and an angiotensin II antagonist have been observed in sodium-depleted normotensive volunteers and in patients with congestive heart failure. Sodium 197-203 renin Homo sapiens 69-74 10726708-2 2000 Inhibition by xenobiotics such as liquorice or mutations in the HSD11 B2 gene, as occur in the rare monogenic hypertensive syndrome of apparent mineralocorticoid excess (AME), result in a compromised 11 betaHSD2 enzyme activity, which in turn leads to overstimulation of the MR by cortisol, sodium retention, hypokalaemia, low plasma renin and aldosterone concentrations, and hypertension. Sodium 291-297 renin Homo sapiens 334-339 10981140-3 2000 Activation of the renin-angiotensin and sympathetic nervous systems and physical compression of the kidneys appear to contribute to obesity-induced increases in sodium reabsorption and hypertension. Sodium 161-167 renin Homo sapiens 18-23 10677399-15 2000 There is thus tentative support for renin profiling in targeting ACE inhibitors to the most deserving, by showing that short term sodium retention does not occur in low renin patients if ACE inhibitors are withdrawn. Sodium 130-136 renin Homo sapiens 36-41 10790760-5 2000 As cardiac diseases progress, the heart dilates, plasma norepinephrine increases, atrial natriuretic factor is released and the renin-angiotensin-aldosterone system is suppressed to maintain water and sodium excretion. Sodium 201-207 renin Homo sapiens 128-133 10790760-7 2000 In more advanced stages, atrial natriuretic factor suppression of the renin-angiotensin-aldosterone system is overridden by overt sympathetic activation and sodium and water retention ensues. Sodium 157-163 renin Homo sapiens 70-75 11055473-10 2000 As expected the activity of the renin-angiotensin-aldosterone system was decreased by enhancing sodium intake but with both low and high sodium intake plasma renin concentration was significantly higher in OH than in ON. Sodium 96-102 renin Homo sapiens 32-37 10489382-12 1999 The factors that mediate enhanced adrenal response to Ang II with sodium restriction may be defective, suggesting the existence of alternative physiological mechanisms for sodium homeostasis in the low-renin state. Sodium 172-178 renin Homo sapiens 202-207 10601066-1 2000 BACKGROUND: The renin-angiotensin system may be implicated in the subtle sodium handling abnormality in preascitic cirrhosis. Sodium 73-79 renin Homo sapiens 16-21 10842655-3 1999 The mechanisms responsible for increased sodium reabsorption and altered pressure natriuresis in obesity include activation of the renin-angiotension and sympathetic nervous systems, and physical compression of the kidneys due to accumulation of intrarenal fat and extracellular matrix. Sodium 41-47 renin Homo sapiens 131-136 10818397-5 2000 The renin-angiotensin-aldosterone system is a major determinant of sodium balance in pregnancy. Sodium 67-73 renin Homo sapiens 4-9 10583449-1 1999 BACKGROUND: In essential hypertension an elevated renal vascular resistance (RVR) may be a marker of renin-angiotensin-aldosterone system-mediated impairment of renal sodium excretion. Sodium 167-173 renin Homo sapiens 101-106 10601129-1 1999 The renin-angiotensin system is a major regulator of body sodium, predominantly through the actions of intrarenal angiotensin II of unclear origin. Sodium 58-64 renin Homo sapiens 4-9 10601129-3 1999 Furthermore, we demonstrate that renin is expressed and secreted in a restricted nephron segment, the connecting tubule, also in a sodium-dependent fashion. Sodium 131-137 renin Homo sapiens 33-38 10601129-4 1999 A paracrine renin-angiotensin system operating along the entire nephron may contribute to long-term arterial pressure regulation by integrating distant tubular sodium-reabsorbing functions. Sodium 160-166 renin Homo sapiens 12-17 10517915-8 1999 In the patient group there was an inverse correlation between: (a) absolute distal sodium reabsorption and active renin (r -0.59, p<0.05); (b) fractional distal sodium reabsorption and sodium excretion (r -0.66, p<0.03). Sodium 83-89 renin Homo sapiens 114-119 10067792-6 1999 RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Sodium 9-15 renin Homo sapiens 56-61 10205239-8 1999 During high sodium intake, plasma renin activity and aldosterone decreased and plasma atrial natriuretic peptide increased; these changes did not correlate with the change in mean arterial pressure, insulin resistance, or change in urinary nitrate excretion. Sodium 12-18 renin Homo sapiens 34-39 10205241-9 1999 Plasma renin levels, measured in 20 patients, were elevated in most cases and correlated inversely (r=-0.63, P<0.01) with the plasma sodium concentration. Sodium 136-142 renin Homo sapiens 7-12 10213527-4 1999 This feedback inhibition for renin release and suppression of aldosterone is reduced with normal sodium intake. Sodium 97-103 renin Homo sapiens 29-34 10051289-2 1999 Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completely suppresses the activated renin-angiotensin system than either intervention alone in sodium-depleted normal individuals. Sodium 174-180 renin Homo sapiens 115-120 10067792-1 1999 OBJECTIVE: Sodium depletion stimulates the renin-angiotensin and sympathetic nervous systems, which may affect the role of each of these systems in the regulation of vascular tone. Sodium 11-17 renin Homo sapiens 43-48 10067792-6 1999 RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Sodium 9-15 renin Homo sapiens 150-155 9922372-4 1999 The process of adaptation is associated with various changes in genetic expression, including a general activation that causes hypertrophy, isogenic shifts which result in the appearance of a slow isomyosin, and a new Na+-K+-ATPase with a low affinity for sodium, reactivation of genes encoding for atrial natriuretic factor and the renin-angiotensin system, and a diminished concentration of sarcoplasmic reticulum Ca2+-ATPase, beta-adrenergic receptors, and the potassium channel responsible for transient outward current. Sodium 256-262 renin Homo sapiens 333-338 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 23-29 renin Homo sapiens 142-147 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 267-273 renin Homo sapiens 142-147 9931123-3 1999 However, only the plasma renin level responds to changes in blood pressure and sodium balance to maintain blood pressure homeostasis. Sodium 79-85 renin Homo sapiens 25-30 9848775-5 1998 In hREN without controlled renal function, urine flow and sodium excretion increased from 13 to 169 microl/min per g kidney wet weight (kwt) and from 1 to 30 micromol/min per g kwt, respectively, as renal perfusion pressure was increased from 67 to 135 mmHg. Sodium 58-64 renin Homo sapiens 3-7 9822438-4 1998 With sodium restriction, plasma renin activity rose from 0.65 to 3.03 ng. Sodium 5-11 renin Homo sapiens 32-37 9853270-2 1998 Several lines of evidence have shown that renin gene expression and release are up-regulated by beta-adrenergic stimulation, sodium depletion, and angiotensin converting enzyme inhibition, but down-regulated by cytokines. Sodium 125-131 renin Homo sapiens 42-47 9719044-5 1998 A sodium-deficient diet, angiotensin-converting enzyme inhibition, and beta1-adrenergic stimulation each increased both human and mouse plasma renin concentration significantly, whereas elevated blood pressure and/or increased plasma angiotensin II levels suppressed them. Sodium 2-8 renin Homo sapiens 143-148 9679045-7 1998 CONCLUSIONS: In preascitic cirrhosis, sodium retention occurs in response to lower body negative pressure, which was associated with increased renal renin-angiotensin activity. Sodium 38-44 renin Homo sapiens 149-154 9679045-8 1998 Stimulation of the intrarenal renin-angiotensin system may be the initial renal pathophysiological change causing sodium retention in cirrhosis. Sodium 114-120 renin Homo sapiens 30-35 9591752-3 1998 A negative sodium balance was present throughout the diet and was associated with a moderate reduction in plasma volume, a marked activation of the renin-aldosterone system, and a concomitant reduction in C- and N-terminal ANF prohormone levels. Sodium 11-17 renin Homo sapiens 148-153 9582047-10 1998 In plasma, the renin level increased 3.6-fold (P<.001), and the aldosterone level increased 3.2-fold (P<.001); the increases were proportional to the degree of sodium reduction for both renin (r=0.66; P<.001) and aldosterone (r=0.64; P<.001). Sodium 166-172 renin Homo sapiens 15-20 9603530-1 1998 BACKGROUND: The renin-angiotensin system regulates blood pressure through its effects on vascular tone, renal hemodynamics, and renal sodium and fluid balance. Sodium 134-140 renin Homo sapiens 16-21 9612329-9 1998 The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin. Sodium 110-116 renin Homo sapiens 218-223 9495269-0 1998 Human vascular renin-angiotensin system and its functional changes in relation to different sodium intakes. Sodium 92-98 renin Homo sapiens 15-20 9605385-4 1998 In the normotensive group prekallikrein levels and renin activity correlated negatively with urinary sodium and chloride excretion during basal conditions and partially during the infusion. Sodium 101-107 renin Homo sapiens 51-56 9773124-1 1998 The renin-angiotensin system is involved in the control of sodium and water balance, mitogenesis and the regulation of vascular tone as well as of the activity of the sympathetic nervous system. Sodium 59-65 renin Homo sapiens 4-9 9495269-7 1998 In high sodium diet subjects, plasma renin activity decreased, and de novo Ang I and Ang II formation by forearm vascular tissue increased to 22 and 14 fmol x 100 mL(-1) x min(-1), respectively (P<.01). Sodium 8-14 renin Homo sapiens 37-42 9417150-12 1998 CONCLUSION: The data suggest that patients with CF are so successful in compensating for volume depletion by vigorous activation of the renin-angiotensin system that salt depletion/dehydration cannot be recognized easily by routine clinical measurements, eg, capillary refill, serum sodium levels, or tachycardia. Sodium 283-289 renin Homo sapiens 136-141 9559415-8 1998 Thus, the renin-angiotensin-aldosterone axis may contribute to cardiorenal hemodynamics and renal sodium handling in patients with mild CHF. Sodium 98-104 renin Homo sapiens 10-15 9369279-0 1997 Sensitivity of blood pressure and renin activation during sodium restriction. Sodium 58-64 renin Homo sapiens 34-39 9532514-2 1997 Blocking this enzymatic cascade has been the focus of considerable research to the extent that the renin-angiotensin system is implicated in the control of blood pressure, sodium and water homeostasis, and cardiovascular function and structure. Sodium 172-178 renin Homo sapiens 99-104 9534323-1 1997 Renin-angiotensin system promotes sodium and chloride retention, participates in the defense response to hypovolemia and, in congestive heart failure, contributes to edema formation and progression of the disease. Sodium 34-40 renin Homo sapiens 0-5 9369279-1 1997 The objective of the present study was to explore the interrelationships among cumulative sodium loss, renin activation, and blood pressure changes during sodium restriction in essential hypertensive patients. Sodium 155-161 renin Homo sapiens 103-108 9369279-2 1997 Specifically, we wanted to know whether the degree of sodium sensitivity of blood pressure depends on renin activation during steady state or on initial renin activation during the first days of sodium restriction. Sodium 54-60 renin Homo sapiens 102-107 9369279-7 1997 Baseline sodium excretion and the activation of renin during the first 3 days both appeared to be predictors of total sodium loss after 7 days. Sodium 118-124 renin Homo sapiens 48-53 9369279-8 1997 Changes in blood pressure were not related to changes in sodium balance, but they were to baseline blood pressure, baseline norepinephrine, and renin activation during the early phase of sodium restriction. Sodium 187-193 renin Homo sapiens 144-149 9369279-9 1997 In addition, blood pressure appeared to fall more when the normal relationship between sodium loss and early (but not late) activation of renin was disturbed. Sodium 87-93 renin Homo sapiens 138-143 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 39-45 renin Homo sapiens 7-12 9338654-3 1997 METHODS: Excretion rates of sodium and water were correlated with the excretion of urodilatin and with circulating levels of atrial natriuretic factor, antidiuretic hormone, aldosterone, and plasma renin activity during a period of 16 hours in 12 patients having had coronary artery bypass operations and with approximately a 400% elevation in levels of atrial natriuretic factor. Sodium 28-34 renin Homo sapiens 198-203 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 39-45 renin Homo sapiens 64-69 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 162-168 renin Homo sapiens 7-12 9139340-3 1997 Activation of the renin-angiotensin-aldosterone system contributes to progression to heart failure by at least two mechanisms: (1) increased left ventricular loading conditions due to vasoconstriction and retention of sodium; (2) direct effects on the myocardium resulting in myocyte hypertrophy and interstitial fibrosis. Sodium 218-224 renin Homo sapiens 18-23 9247766-5 1997 The combination of captopril 50 mg and losartan 50 mg had additive effects on blood pressure fall and renin release in sodium-depleted normotensive subjects. Sodium 119-125 renin Homo sapiens 102-107 9041252-7 1997 CONCLUSIONS: In cirrhosis, sinusoidal portal hypertension and an activated renin-angiotensin-aldosterone system seem to be important in the pathogenesis of sodium retention. Sodium 156-162 renin Homo sapiens 75-80 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 renin Homo sapiens 36-41 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 renin Homo sapiens 51-56 9048137-11 1997 Plasma renin activity and aldosterone are generally elevated at landing, consistent with sodium retention, but inflight levels have been variable. Sodium 89-95 renin Homo sapiens 7-12 9022564-4 1997 Ischemic and nephrotoxic injuries are induced more readily in sodium-depleted animals and patients because of impaired renal hemodynamics and activation of the renin-angiotensin system. Sodium 62-68 renin Homo sapiens 160-165 9022564-10 1997 Finally, there is evidence that activation of the renin-angiotensin system by sodium depletion will enhance the growth of cysts in animal models of cystic renal disease. Sodium 78-84 renin Homo sapiens 50-55 9040450-1 1997 The combination of single oral doses of an angiotensin I-converting enzyme inhibitor (captopril) and a type 1 angiotensin II receptor antagonist (losartan) has additive effects on blood pressure fall and renin release in sodium-depleted normotensive subjects. Sodium 221-227 renin Homo sapiens 204-209 8621146-6 1996 Sodium restriction resulted in less weight loss in the cirrhotic patients (P = .03), with significantly lower plasma renin activity (P = .001). Sodium 0-6 renin Homo sapiens 117-122 8994730-1 1997 The renin-angiotensin system regulates blood pressure and sodium homeostasis through a series of coordinated substrate-enzyme interactions. Sodium 58-64 renin Homo sapiens 4-9 8983669-8 1996 There is little doubt that an inappropriately high plasma (and tissue) level of renin, related to sodium balance, is associated with increased left ventricular hypertrophy and cardiovascular complications. Sodium 98-104 renin Homo sapiens 80-85 9004086-6 1996 Renal abnormalities that cause salt-insensitive hypertension are characterized by normal functional kidney mass, and the ability to appropriately modulate the renin-angiotensin system during changes in sodium intake; important causes of salt-insensitive hypertension include widespread increases in preglomerular resistance and increased reabsorption in the proximal tubules and loops of Henle. Sodium 202-208 renin Homo sapiens 159-164 8934386-7 1996 Sodium sensitivity is commonly observed in these patients, so that low doses of diuretics correct the increased pulse pressure, particularly in those with normal or low plasma renin activity. Sodium 0-6 renin Homo sapiens 176-181 8790265-2 1996 The renin-angiotensin-aldosterone system, the sympathetic nervous system, and arginine vasopressin are responsible for sodium and water retention in patients with cirrhosis. Sodium 119-125 renin Homo sapiens 4-9 8870314-14 1996 CONCLUSION: This study shows ethnic differences in renin-sodium profile and renal PG synthesis, during changes in dietary sodium. Sodium 57-63 renin Homo sapiens 51-56 8870314-14 1996 CONCLUSION: This study shows ethnic differences in renin-sodium profile and renal PG synthesis, during changes in dietary sodium. Sodium 122-128 renin Homo sapiens 51-56 9050972-0 1997 An abnormal sodium metabolism in Japanese patients with essential hypertension, judged by serum sodium distribution, renal function and the renin-aldosterone system. Sodium 12-18 renin Homo sapiens 140-145 8941579-7 1996 Plasma renin and aldosterone were significantly elevated in the symptomatic children, and strongly correlated with all parameters of tubule sodium reabsorption. Sodium 140-146 renin Homo sapiens 7-12 8815755-10 1996 RESULTS: Sodium restriction was associated with a mean decrease (+/- one half of the 95% CI) in plasma sodium levels of 0.9 +/- 0.9 mmol/L from a mean of 139.3 mmol/L during the baseline cycle (P = 0.018), a decrease in urinary sodium excretion of 40.3 +/- 18 mmol/d from a mean of 117 mmol/d during the baseline cycle (P = 0.001), and an increase in plasma renin activity of 0.14 +/- 0.08 ng/(L . Sodium 9-15 renin Homo sapiens 358-363 9076343-8 1996 GH causes sodium retention which occurs in part through activation of the renin-angiotensin system. Sodium 10-16 renin Homo sapiens 74-79 8895036-1 1996 The aims of the present study were to investigate the effects of changes in sodium intake in patients with untreated mild essential hypertension on the hormonal (plasma renin activity and aldosterone) and renal tubular responses to short-term hyperinsulinemia as achieved by an oral glucose tolerance test (OGTT). Sodium 76-82 renin Homo sapiens 169-174 8671370-0 1996 The influence of dietary sodium restriction on renal and ovarian renin and prorenin production during ovarian stimulation. Sodium 25-31 renin Homo sapiens 65-70 8671370-1 1996 In a prospective study, the effect of dietary sodium restriction on plasma and follicular fluid renin and prorenin concentrations and on fertilization measures was investigated during ovarian stimulation. Sodium 46-52 renin Homo sapiens 96-101 8671370-3 1996 Plasma renin and prorenin concentrations were higher in the low sodium than in the normal sodium group. Sodium 64-70 renin Homo sapiens 7-12 8671370-3 1996 Plasma renin and prorenin concentrations were higher in the low sodium than in the normal sodium group. Sodium 90-96 renin Homo sapiens 7-12 8931343-1 1996 Renin-angiotensin system plays a prominent role in the sodium and water homeostasis. Sodium 55-61 renin Homo sapiens 0-5 8894667-6 1996 Thus we studied the response of the renin-angiotensin-aldosterone system to sodium depletion using a single dose of furosemide. Sodium 76-82 renin Homo sapiens 36-41 8567042-0 1996 Does the renin-angiotensin system determine the renal and systemic hemodynamic response to sodium in patients with essential hypertension? Sodium 91-97 renin Homo sapiens 9-14 8567042-3 1996 Our aim was to clarify the role of the renin-angiotensin system in the renal and systemic adaptation to a change in dietary sodium. Sodium 124-130 renin Homo sapiens 39-44 8567042-15 1996 renin-angiotensin system response to increased sodium intake. Sodium 47-53 renin Homo sapiens 0-5 8629540-1 1996 Pharmacologic agents that attenuate the influence of the renin-angiotensin-aldosterone system are known to reduce systemic arterial blood pressure through vasodilatory action and enhanced renal clearance of sodium and water. Sodium 207-213 renin Homo sapiens 57-62 8635674-9 1996 Combining all patients, there were relevant associations between changes of urinary sodium excretion and blood volume (Spearman correlation coefficient r = 0.57), blood pressure and angiotensin II (diastolic: r = -0.7; systolic: r = -0.48), and exchangeable body sodium and renin activity (r = -0.5). Sodium 84-90 renin Homo sapiens 274-279 8867564-4 1996 Assessment of plasma renin activity (PRA) related to concurrent 24 h sodium excretion was used to define patients with high (n = 12), medium (n = 16) and low renin profile (n = 8). Sodium 69-75 renin Homo sapiens 21-26 8894667-13 1996 During sodium depletion with furosemide, renin as well as aldosterone levels rose significantly in 1 parent and a sibling, respectively. Sodium 7-13 renin Homo sapiens 41-46 7641363-12 1995 CONCLUSIONS: The combined administration of a standard single oral dose of an ACE inhibitor and an Ang II antagonist to mildly sodium-depleted normal subjects (1) had a major additive effect on plasma renin rise, (2) induced an additional mean blood pressure reduction, and (3) had no additive effect on plasma aldosterone fall. Sodium 127-133 renin Homo sapiens 201-206 8551200-3 1996 Assessment of plasma renin activity (PRA) related to urinary sodium excretion was used to define subgroups with high (n = 12), medium (n = 16) and low renin profiles (n = 8). Sodium 61-67 renin Homo sapiens 21-26 8554732-1 1995 Plasma active renin consists of multiple glycoforms, which are differentially stored and secreted by the kidney, have varying plasma half-lives, and appear to have differing effects on renal sodium and water metabolism. Sodium 191-197 renin Homo sapiens 14-19 7635961-1 1995 The renin-angiotensin system regulates blood pressure and sodium balance. Sodium 58-64 renin Homo sapiens 4-9 7611241-10 1995 The results of the present analysis show that acute water loading per se may enhance renal sodium excretion and hence modify the level of activity of the renin-angiotensin system expected from a given sodium diet. Sodium 201-207 renin Homo sapiens 154-159 7752314-5 1995 Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p < 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p < 0.05 to < 0.01) in the adrenalectomy group. Sodium 79-85 renin Homo sapiens 126-131 7662248-1 1995 Both a high renin-sodium profile and abnormal levels of sex hormones have been linked to myocardial infarction (MI) in men. Sodium 18-24 renin Homo sapiens 12-17 7473515-1 1995 The renin-angiotensin-aldosterone hormonal servo-control system plays a major role in defending normotension and sodium and potassium balance. Sodium 113-119 renin Homo sapiens 4-9 7473515-2 1995 Derangements of the system involving either excess renin-angiotensin vasoconstriction or too much sodium-volume retention for the plasma-renin level can be implicated in sustaining the hypertension of most human hypertensive disorders. Sodium 98-104 renin Homo sapiens 137-142 7784414-5 1995 Renin and aldosterone levels were found increased in group C. Systemic vascular resistance differed significantly in the three groups, being lower in group C. Significant higher values in the Doppler reverse/forward ratio were observed in patients with markedly increased sodium retention and less systemic vascular resistance (group C). Sodium 272-278 renin Homo sapiens 0-5 7833591-1 1994 The renin-angiotensin-aldosterone system (RAAS) is one of the main systems involved in the regulation of blood pressure and sodium homeostasis. Sodium 124-130 renin Homo sapiens 4-9 7600052-1 1995 Both a retrospective and a prospective study of hypertensive patients have detected a significant positive relationship between pretreatment renin and sodium profiles, and the occurrence of coronary artery disease events during treatment. Sodium 151-157 renin Homo sapiens 141-146 7534728-2 1994 Nitric oxide has also been implicated in the control of the secretion of hormones by the pancreas, hypothalamus, and anterior pituitary gland, and evidence is accumulating that it contributes to the regulation of the secretion of renin and vasopressin, hormones that play key roles in the control of sodium and water balance. Sodium 300-306 renin Homo sapiens 230-235 7792315-1 1995 The renin-angiotensin system is intimately involved in the control of sodium and water balance, the activity of the sympathetic nervous system, mitogenesis and the regulation of vascular tone. Sodium 70-76 renin Homo sapiens 4-9 7792804-7 1995 To further elucidate the pattern of inheritance we studied the response of the renin-angiotensin-aldosterone system to the stimulation by sodium depletion in the familial autosomal dominant form and in two families with sporadic cases. Sodium 138-144 renin Homo sapiens 79-84 8141158-2 1994 To elucidate the role of a mechanism responsible for renal sodium reabsorption on the time-course of renin suppression, 16 young borderline hypertensive patients were studied by analyzing the relationship between the level of baseline activation of lymphocyte Na+:H+ exchange and the degree of plasma renin activity (PRA) suppression in response to saline loading. Sodium 59-65 renin Homo sapiens 101-106 7531080-1 1994 Secretion and synthesis of renin are stimulated by the lack of angiotensin II and by a low sodium intake. Sodium 91-97 renin Homo sapiens 27-32 7531084-2 1994 They appear to be linked particularly by the renin angiotensin system and the control of sodium balance. Sodium 89-95 renin Homo sapiens 45-50 8156731-15 1994 An increased plasma renin activity associated with the lack of blood pressure rise would reinforce sodium and water retention. Sodium 99-105 renin Homo sapiens 20-25 7861706-8 1994 During chronically higher sodium intake, serum ANP was significantly higher (median 130 vs. 81 ng/liter, P = 0.0006) and plasma renin tended to be higher (median 20.5 vs. 13.5, P = 0.08) in ADPKD than in control subjects. Sodium 26-32 renin Homo sapiens 128-133 7825084-3 1994 Renin profiles, obtained by the plotting of PRA against the urinary excretion of sodium, showed a 62% prevalence of low-renin hypertension, the remaining 38% of the patients having normal-renin hypertension. Sodium 81-87 renin Homo sapiens 0-5 8124802-7 1994 Suppression of plasma renin activity and aldosterone by high-sodium diet was blunted in cardiac transplant recipients compared with healthy subjects (respectively, plasma renin activity: 1.41 +/- 0.30 versus 0.68 +/- 0.21 ng.mL-1 x h-1, P < .05; aldosterone: 391 +/- 35 versus 166 +/- 21 pmol/L, P < .05). Sodium 61-67 renin Homo sapiens 22-27 8124802-7 1994 Suppression of plasma renin activity and aldosterone by high-sodium diet was blunted in cardiac transplant recipients compared with healthy subjects (respectively, plasma renin activity: 1.41 +/- 0.30 versus 0.68 +/- 0.21 ng.mL-1 x h-1, P < .05; aldosterone: 391 +/- 35 versus 166 +/- 21 pmol/L, P < .05). Sodium 61-67 renin Homo sapiens 171-176 8141158-5 1994 These findings suggest that a mechanism influencing renal sodium reabsorption as Na+:H+ exchange could also affect the control of plasma renin activity, and concur with the development of salt-sensitive high blood pressure. Sodium 58-64 renin Homo sapiens 137-142 8021469-8 1994 Among the subjects with a low or normal renin-sodium profile, 1% (one of 82) had a false-positive result. Sodium 46-52 renin Homo sapiens 40-45 8021469-6 1994 Renin responses were analyzed according to baseline renin-sodium profile. Sodium 58-64 renin Homo sapiens 52-57 8153287-9 1994 Reversed sodium rhythm was associated with reversed circadian rhythms for GFR, effective renal plasma flow and urine flow, and blunting or reversal of the day-night differences in blood pressure and plasma renin activity. Sodium 9-15 renin Homo sapiens 206-211 8021469-6 1994 Renin responses were analyzed according to baseline renin-sodium profile. Sodium 58-64 renin Homo sapiens 0-5 8304017-12 1994 CONCLUSION: The results suggest that the competitive relationship between ANP and the renin-aldosterone system in regulating sodium balance and fluid volume is preserved during pregnancy. Sodium 125-131 renin Homo sapiens 86-91 7954533-6 1994 Activation of the renin-angiotensin system favours the proximal tubular reabsorption of sodium and water, which may result in dilutional hyponatraemia. Sodium 88-94 renin Homo sapiens 18-23 8112708-1 1993 The renin-angiotensin system (RAS) is known as a system which constricts vessels and enhances renal retention of sodium and water to raise the blood pressure. Sodium 113-119 renin Homo sapiens 4-9 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 10-15 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 219-224 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 219-224 8134255-6 1993 Serum aldosterone levels (P < 0.01) as well as serum renin levels (P < 0.05) significantly decreased with increasing sodium intake. Sodium 123-129 renin Homo sapiens 56-61 8376285-7 1993 We suggest that the combined effect of the sustained suppressions of plasma renin activity and plasma aldosterone and norepinephrine concentrations constitutes a mechanism of the increase in renal sodium excretion. Sodium 197-203 renin Homo sapiens 76-81 8514035-1 1993 BACKGROUND: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive, antinatriuretic forces such as the renin aldosterone angiotensin system and the sympathetic nervous system, and vasodilatory, natriuretic agents such as atrial natriuretic factor (ANF). Sodium 12-18 renin Homo sapiens 139-144 8006915-3 1994 Compared with whites plasma renin is low in blacks independently of age, the level of BP and dietary sodium consumption. Sodium 101-107 renin Homo sapiens 28-33 8500861-6 1993 When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators. Sodium 50-56 renin Homo sapiens 122-127 8228194-5 1993 Severe sodium restriction increased plasma renin activity and noradrenaline concentration, as well as serum total and low-density lipoprotein-cholesterol and triglycerides. Sodium 7-13 renin Homo sapiens 43-48 8503435-5 1993 Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II, and aldosterone has been demonstrated in diabetic renal disease. Sodium 10-16 renin Homo sapiens 64-69 8324299-6 1993 The activation of the renin-aldosterone system in newborns and infants probably represents an important physiological mechanism designed to maintain positive sodium balance. Sodium 158-164 renin Homo sapiens 22-27 8397245-11 1993 At the end of the low-sodium phase there was a significant increase in plasma renin activity and aldosterone levels, but no change in plasma electrolytes. Sodium 22-28 renin Homo sapiens 78-83 8324299-8 1993 The superimposition of a disease process, or the injudicious prescription of a drug, inhibiting renin release or angiotensin II production, could theoretically facilitate sodium wasting in newborns or infants, or precipitate hyporeninaemic hypoaldosteronism in older adults. Sodium 171-177 renin Homo sapiens 96-101 7685442-3 1993 On the study day, 24-h urinary sodium excretion was approximately 10-20 mmol Na, with an increase in renin and aldosterone levels at baseline. Sodium 31-37 renin Homo sapiens 101-106 8386932-2 1993 In short term infusion studies (2 or 8 h duration), ANF plasma levels as observed after sodium loading (50-70 pg/ml) lowered basal renin (PRA) and aldosterone, but had only a marginal effect on angiotensin II-stimulated aldosterone secretion. Sodium 88-94 renin Homo sapiens 131-136 8350592-8 1993 In one sibling negative values may have been caused by suppression of the renin-angiotensin-system due to high sodium replacement therapy. Sodium 111-117 renin Homo sapiens 74-79 8104577-0 1993 Renin suppressibility and blood pressure response during acute sodium loading in patients with essential hypertension. Sodium 63-69 renin Homo sapiens 0-5 8489125-2 1993 In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. Sodium 143-149 renin Homo sapiens 21-26 8489125-2 1993 In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. Sodium 241-247 renin Homo sapiens 21-26 8489125-3 1993 The suppression of some renal depressor-natriuretic systems, the dopaminergic, kallikrein-kinin and prostaglandin E2 systems may contribute to the retention of sodium-water in these patients, because these depressor systems were observed to be greatly suppressed in essential hypertension, especially in the low renin group. Sodium 160-166 renin Homo sapiens 312-317 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 22-28 renin Homo sapiens 4-9 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 69-75 renin Homo sapiens 4-9 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 69-75 renin Homo sapiens 4-9 8471406-1 1993 A combination of dietary sodium restriction (40 mmol day-1) and frusemide pretreatment has been used to activate the renin angiotensin system (RAS) in order to characterise the haemodynamic and hormonal responses to enalapril in young normotensives. Sodium 25-31 renin Homo sapiens 117-122 8098306-1 1993 Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. Sodium 181-187 renin Homo sapiens 108-113 8498972-3 1993 Normally, in the presence of hypertension or sodium-volume excess, plasma renin activity promptly falls to zero. Sodium 45-51 renin Homo sapiens 74-79 8498972-8 1993 These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Sodium 34-40 renin Homo sapiens 28-33 8498972-8 1993 These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Sodium 157-163 renin Homo sapiens 28-33 8498973-0 1993 Acute effects of a pseudo-tetrapeptide as renin inhibitor on blood pressure and renin-angiotensin system of sodium-repleted and sodium-depleted hypertensive patients. Sodium 108-114 renin Homo sapiens 42-47 8498973-0 1993 Acute effects of a pseudo-tetrapeptide as renin inhibitor on blood pressure and renin-angiotensin system of sodium-repleted and sodium-depleted hypertensive patients. Sodium 108-114 renin Homo sapiens 80-85 8098306-11 1993 For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Sodium 31-37 renin Homo sapiens 96-101 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 102-107 8458606-4 1993 Urinary sodium excretion after glucose ingestion was lower in CGN than in C. These data demonstrated that the glucose-induced renin-angiotensin-aldosterone system in patients with chronic renal disease differed from that in healthy subjects. Sodium 8-14 renin Homo sapiens 126-131 8443481-11 1993 The aldosterone to active renin ratio was decreased by angiotensin I converting enzyme inhibition and increased by sodium depletion, showing treatment efficacy. Sodium 115-121 renin Homo sapiens 26-31 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 83-88 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 102-107 8382130-13 1993 Thus, the biosynthesis and secretion of renal human renin in these transgenic mice are obviously stimulated by sodium depletion. Sodium 111-117 renin Homo sapiens 52-57 8302404-4 1993 In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production. Sodium 108-114 renin Homo sapiens 208-213 8322536-5 1993 Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). Sodium 58-64 renin Homo sapiens 200-205 8322536-5 1993 Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). Sodium 58-64 renin Homo sapiens 306-311 1457079-0 1992 Relationship of the renin-angiotensin system and systemic arterial pressure to sodium excretion during atrial natriuretic peptide infusion in men. Sodium 79-85 renin Homo sapiens 20-25 1300562-3 1992 The aim of the study was to determine whether and in what extent patients with HA and healthy subjects differ in EPO secretion and whether EPO serum level is related in this patients to renin response to dietary sodium restriction and upright position of the body. Sodium 212-218 renin Homo sapiens 186-191 1460897-0 1992 [Influence of arterial pressure and plasma renin activity on tubular reabsorption of sodium]. Sodium 85-91 renin Homo sapiens 43-48 1516945-3 1992 As the major regulator of arterial blood pressure and sodium balance, the renin axis supports normotension or hypertension via angiotensin-mediated vasoconstriction and angiotensin plus aldosterone-induced renal sodium retention. Sodium 54-60 renin Homo sapiens 74-79 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 37-43 renin Homo sapiens 14-19 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 37-43 renin Homo sapiens 148-153 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 166-172 renin Homo sapiens 14-19 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 23-28 1388962-0 1992 The influence of age on renal function and renin and aldosterone responses to sodium-volume expansion and contraction in normotensive and mildly hypertensive humans. Sodium 78-84 renin Homo sapiens 43-48 1582493-2 1992 During the first month of life, increased retention of sodium is present in the SHR which appears to be mediated by the renin-angiotensin system. Sodium 55-61 renin Homo sapiens 120-125 1532566-2 1992 Recumbent plasma renin activity was low during normal sodium intake (135 mmol daily), and the response to upright posture or to low sodium diet (10 mmol daily) was blunted. Sodium 54-60 renin Homo sapiens 17-22 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 76-81 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 76-81 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 239-245 renin Homo sapiens 23-28 1538559-12 1992 As with the weight loss diet, patients on a low sodium/high potassium diet in the highest baseline renin index quartile had a greater reduction in DBP than patients in the lowest baseline renin index quartile. Sodium 48-54 renin Homo sapiens 99-104 1538559-12 1992 As with the weight loss diet, patients on a low sodium/high potassium diet in the highest baseline renin index quartile had a greater reduction in DBP than patients in the lowest baseline renin index quartile. Sodium 48-54 renin Homo sapiens 188-193 1633072-7 1992 Activity of the renin-angiotensin system is associated with sodium and water retention and plasma volume expansion. Sodium 60-66 renin Homo sapiens 16-21 1387480-2 1992 It has been assumed that restricted sodium excretion with the kidneys during fasting is mainly caused by activation of the renin-angiotensin-aldosterone system, with ANP contributing to it, insulin not playing the major role in this process. Sodium 36-42 renin Homo sapiens 123-128 1735598-5 1992 The renin-angiotensin-aldosterone system was significantly less activated with women in the supine position in pregnancy-induced hypertensive and chronic hypertensive women; however, as opposed to pregnancy-induced hypertensive women, those with chronic hypertension reassumed their humoral response to upright posture, which was accompanied by a significant reduction in sodium excretion. Sodium 372-378 renin Homo sapiens 4-9 1805062-2 1991 The results obtained showed that not only the increased function of the renin-angiotensin-aldosterone system, but the higher activity of the sympathoadrenal system in the presence of weakened adrenocortical glucocorticoid and epiphyseal functions late in CCI played a role in the mechanisms responsible for sodium retention in the patients with the disease. Sodium 307-313 renin Homo sapiens 72-77 1728438-2 1992 BACKGROUND: The participation of the renin-angiotensin system in the control of blood pressure in normal, sodium-replete subjects is not clear. Sodium 106-112 renin Homo sapiens 37-42 1761331-8 1991 However, in the erect position, which is associated with even further increases in activity of the renin angiotensin aldosterone system, the reduction in diuresis and natriuresis that a fall in glomerular filtration rate would cause is offset by abolition of the rise in sodium retaining hormones, angiotensin II and aldosterone that mediate the antinatriuretic effect of the erect position. Sodium 271-277 renin Homo sapiens 99-104 1330385-1 1992 19-hydroxy-androstenedione (19-OH-A), a C19 steroid, is an amplifier of the sodium retaining action of aldosterone under the control of ACTH and renin-angiotensin system. Sodium 76-82 renin Homo sapiens 145-150 1493845-3 1992 Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. Sodium 81-87 renin Homo sapiens 7-12 1835959-7 1991 Plasma renin activity was suppressed by treatment on the low but not on the high sodium diet (p less than 0.05). Sodium 81-87 renin Homo sapiens 7-12 1836003-0 1991 ANF and the renin-angiotensin system in the regulation of sodium balance: longitudinal studies in experimental heart failure. Sodium 58-64 renin Homo sapiens 12-17 1836003-1 1991 Over the last three decades the role of the renin-aldosterone axis for the renal conservation of sodium has become well established. Sodium 97-103 renin Homo sapiens 44-49 1836003-3 1991 Evidence has been presented to suggest that ANF and the renin-aldosterone axis function in an integrated manner for the regulation of sodium balance, with their primary actions exerted in the postprandial and postabsorptive phases, respectively. Sodium 134-140 renin Homo sapiens 56-61 1741989-4 1991 However, if adequate volume is unavailable because of sodium restriction, sustained activation of the renin-angiotensin system increases blood pressure sufficiently to restore nephron perfusion. Sodium 54-60 renin Homo sapiens 102-107 1838027-2 1991 The present article focuses on the potential importance of ANP (ANF 99-126) in essential hypertension with particular reference to circulating ANP levels and the relationship between the ANP and the renin-angiotensin system in the control of sodium balance and blood pressure. Sodium 242-248 renin Homo sapiens 199-204 1838027-5 1991 This is further supported by studies during alterations in dietary sodium intake, as sodium restriction high-lighted important relationships between ANP and the renin angiotensin system. Sodium 85-91 renin Homo sapiens 161-166 1959244-10 1991 However, high-renin patients generally respond more vigorously, and the hypotensive response is enhanced by sodium depletion. Sodium 108-114 renin Homo sapiens 14-19 1914196-3 1991 The plasma renin value directly reflects the presence and degree of renin-mediated vasoconstriction, and, inversely, defines the predominance of sodium-related vasoconstriction. Sodium 145-151 renin Homo sapiens 11-16 1921483-7 1991 These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD. Sodium 128-134 renin Homo sapiens 37-42 1914196-8 1991 Conversely, low-renin equally hypertensive patients have relatively more sodium volume and are less vasoconstricted; they are generally responsive to natriuretic drugs (e.g., diuretics or calcium antagonists) and appear relatively protected from vascular sequelae such as stroke and heart attack. Sodium 73-79 renin Homo sapiens 16-21 1914203-5 1991 The chief instruments of this strategy are the renin-sodium profile and the response of plasma renin activity and blood pressure to specific antirenin system drugs. Sodium 53-59 renin Homo sapiens 47-52 1914203-10 1991 In our present state of knowledge, the basic diagnostic biochemical workup includes the renin-sodium profile and the 24-h urinary sodium, potassium, and microalbumin excretion rates. Sodium 94-100 renin Homo sapiens 88-93 1837568-9 1991 These results therefore indicated that hypotension caused by hemodynamic alteration and extremely stimulated renin release might effect on proximal tubular sodium reabsorption and GFR, leading to sodium retention and diuretic resistance in cirrhosis. Sodium 156-162 renin Homo sapiens 109-114 1659794-3 1991 Plasma renin activity (PRA) plasma concentration of active renin, atrial natriuretic hormone and urinary cyclic GMP were higher in patients in NYHA Class IV than in those in Classes II-III, whilst plasma sodium, angiotensinogen, prealbumin and retinol-binding protein concentrations were lower in Class IV patients than in patients in Classes II-III. Sodium 204-210 renin Homo sapiens 7-12 1659794-7 1991 The serum sodium was negatively correlated with active renin (r = -0.66, p less than 0.0001) in these patients not receiving converting enzyme inhibitors. Sodium 10-16 renin Homo sapiens 55-60 1833197-2 1991 The important vasoconstrictor, fluid and sodium retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity and vasopressin; the vasodilator, volume and sodium eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins, such as prostacyclin and prostaglandin E2, dopamine, bradykinin and, possibly, endothelium-derived relaxing factor and vasoactive intestinal peptide. Sodium 41-47 renin Homo sapiens 74-79 1833197-5 1991 In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. Sodium 166-172 renin Homo sapiens 34-39 1837568-9 1991 These results therefore indicated that hypotension caused by hemodynamic alteration and extremely stimulated renin release might effect on proximal tubular sodium reabsorption and GFR, leading to sodium retention and diuretic resistance in cirrhosis. Sodium 196-202 renin Homo sapiens 109-114 1647690-0 1991 Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system. Sodium 14-20 renin Homo sapiens 65-70 1830563-9 1991 The blood pressure lowering was due to specific renin inhibition as exemplified by the influence of the kidney, sodium status, species, or stereoselectivity. Sodium 112-118 renin Homo sapiens 48-53 2065475-2 1991 In Gordon"s syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis. Sodium 131-137 renin Homo sapiens 175-180 1873002-5 1991 The decrease in MBP appeared to be significantly higher in sodium-sensitive (11.2 mm Hg, P less than .001) than in sodium-insensitive (5.7 mm Hg, P less than .05) patients and was in salt-sensitive patients significantly correlated to the increase in plasma renin activity (PRA). Sodium 59-65 renin Homo sapiens 258-263 2045142-1 1991 When the function of the renin system is inhibited, blood pressure becomes more dependent on changes in sodium and water balance. Sodium 104-110 renin Homo sapiens 25-30 2029014-6 1991 RESULTS: The low sodium diet resulted in a highly significant increase in the plasma renin (2p = 0.0001), aldosterone (2p = 0.0006), and urinary prostaglandin E2 (2p = 0.01) concentrations and the renal potassium excretion (2p = 0.0009), whereas renal sodium excretion was significantly reduced (2p = 0.0001). Sodium 17-23 renin Homo sapiens 85-90 1826997-0 1991 Importance of the renin-angiotensin system in sodium regulation in essential hypertension. Sodium 46-52 renin Homo sapiens 18-23 1759997-2 1991 METHODS: Renin profiles, obtained by plotting plasma renin activity against the urinary excretion of sodium, were classified as high (12 percent of the subjects), normal (56 percent), and low (32 percent), and there were expected variations according to age, sex, and race. Sodium 101-107 renin Homo sapiens 9-14 1830107-11 1991 However, one explanation for the increase in plasma renin activity and fall in atrial natriuretic peptide is a small reduction in total body sodium. Sodium 141-147 renin Homo sapiens 52-57 1826997-8 1991 These results suggest that the state of the renin-angiotensin system is important in renal sodium excretion in EHT. Sodium 91-97 renin Homo sapiens 44-49 1838244-2 1991 Important vasoconstrictor, fluid- and sodium-retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity, and vasopressin; vasodilator, volume, and sodium-eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins like prostacyclin and prostaglandin E2, dopamine, bradykinin, and possibly, endothelial derived relaxing factor (EDRF). Sodium 38-44 renin Homo sapiens 71-76 1830843-4 1991 Plasma renin activity was inversely related to sodium excretion at both proximal (r = -0.145, P less than 0.05) and distal (r = -0.236, P less than 0.001) tubular site, whereas plasma aldosterone was significantly and inversely related to distal sodium excretion only (r = -0.305, P less than 0.001). Sodium 47-53 renin Homo sapiens 7-12 1830843-4 1991 Plasma renin activity was inversely related to sodium excretion at both proximal (r = -0.145, P less than 0.05) and distal (r = -0.236, P less than 0.001) tubular site, whereas plasma aldosterone was significantly and inversely related to distal sodium excretion only (r = -0.305, P less than 0.001). Sodium 246-252 renin Homo sapiens 7-12 2006991-8 1991 These correlations within renin tertiles occurred even though there were no differences in mean blood pressure, plasma ionized calcium, total plasma protein and plasma sodium across renin categories. Sodium 168-174 renin Homo sapiens 26-31 2009143-5 1991 Nevertheless, they are affected adversely by the discordant renin-angiotensin II arising from the ischemic nephrons" presence, which exerts an unwanted sodium-retaining effect on the proximal tubules of the adapting nephrons. Sodium 152-158 renin Homo sapiens 60-65 1984191-8 1991 Her ratio of plasma renin activity to urinary aldosterone-18-glucuronide excretion was 1.7 after three days of sodium restriction, as compared with a ratio of 4.7 at the age of nine years (normal range, 0.03 to 0.1). Sodium 111-117 renin Homo sapiens 20-25 1838244-5 1991 In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. Sodium 166-172 renin Homo sapiens 34-39 1921246-2 1991 Restriction of salt intake in the diet lowers blood pressure in many subjects with high blood pressure and this fall in blood pressure is mediated in part by a diminished renin response to sodium restriction as hypertension develops. Sodium 189-195 renin Homo sapiens 171-176 1921246-3 1991 The effect of sodium restriction, like diuretics, is additive to many blood pressure lowering drugs, particularly those that inhibit the renin system such as beta-blockers and angiotensin converting enzyme inhibitors. Sodium 14-20 renin Homo sapiens 137-142 1886454-2 1991 Sodium restriction potentiated plasma level of norepinephrine in parallel with an increased plasma renin activity (r = 0.81, F = 31.2, p less than 0.05 given by the percent changes). Sodium 0-6 renin Homo sapiens 99-104 1754319-2 1991 Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity. Sodium 0-6 renin Homo sapiens 137-142 1796634-6 1991 In more severe heart failure vasoconstrictor, sodium and water-retaining mechanisms like the renin-angiotensin-aldosterone system are activated with the consequence of an increase of systemic vascular resistance, a reduction of renal blood flow, and an increased fluid retention. Sodium 46-52 renin Homo sapiens 93-98 1984626-3 1991 A biracial sample of 159 children and adolescents were classified as having a low, intermediate, or high renin-sodium profile based on the relationship between their plasma renin activity and 24-hour urinary sodium excretion. Sodium 111-117 renin Homo sapiens 105-110 1839104-7 1991 Possible mechanisms are a reduced renal perfusion pressure, a receptor down-regulation or an overactivity of sodium-retaining hormones like the renin aldosterone system, and the sympathetic activity. Sodium 109-115 renin Homo sapiens 144-149 2081010-3 1990 In 10 subjects with high renin hypertension, an increase in dietary sodium intake resulted in an increase in urinary calcium excretion (2.5 to 3.4 mmol/L, P = .011) and an increase in serum 1,25-dihydroxyvitamin D (51.2 to 61.0 pmol/L, P = .045). Sodium 68-74 renin Homo sapiens 25-30 2081010-6 1990 It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. Sodium 46-52 renin Homo sapiens 235-240 2244565-2 1990 With an unrestricted sodium diet, plasma renin concentration was inhibited within 10 minutes by intravenous enalkiren and remained essentially undetectable for greater than or equal to 6 hours (11.9 +/- 4 to 1.0 +/- 0.6 ng angiotensin I/ml/hour, p less than 0.05). Sodium 21-27 renin Homo sapiens 41-46 2081010-6 1990 It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. Sodium 46-52 renin Homo sapiens 263-268 2081010-8 1990 Therefore, 1,25-dihydroxyvitamin D may be a mediator in the response of high renin hypertension to increased sodium intake. Sodium 109-115 renin Homo sapiens 77-82 2261144-3 1990 By interfering with the formation of angiotensin II, the active agent of the renin system, ACE inhibitors block the system"s vasoconstrictive and sodium-retaining effects, with a consequent reduction in systemic blood pressure. Sodium 146-152 renin Homo sapiens 77-82 2146863-4 1990 The maximal response of urinary sodium excretion rate after ANF infusion was positively correlated with the basal sodium excretion rate (r = 0.579; p less than 0.05) and inversely correlated with basal plasma renin activity (r = -0.623; p less than 0.05). Sodium 32-38 renin Homo sapiens 209-214 2148092-7 1990 This study demonstrates a marked sensitivity of the responses of both the ANP and the renin-aldosterone system to small changes in sodium intake and points to their importance in the renal adaptations to small alterations in dietary sodium intake. Sodium 131-137 renin Homo sapiens 86-91 2148092-7 1990 This study demonstrates a marked sensitivity of the responses of both the ANP and the renin-aldosterone system to small changes in sodium intake and points to their importance in the renal adaptations to small alterations in dietary sodium intake. Sodium 233-239 renin Homo sapiens 86-91 1962804-0 1990 The effect of the renin inhibitor ES-1005 on the expression of the kidney renin gene in sodium-depleted marmosets. Sodium 88-94 renin Homo sapiens 74-79 1962804-1 1990 The effect of the renin inhibitor ES-1005 or captopril on the expression of the kidney renin gene was investigated in sodium-depleted marmosets. Sodium 118-124 renin Homo sapiens 87-92 1962804-7 1990 These results suggest that the treatment with the renin inhibitor ES-1005 for one week has a paradoxical effect on kidney renin gene expression and renin release from the kidney in sodium-depleted marmosets. Sodium 181-187 renin Homo sapiens 50-55 2097166-0 1990 Effect of sodium depletion on the renin-angiotensin-aldosterone system and renal prostaglandins in acromegalic patients. Sodium 10-16 renin Homo sapiens 34-39 2079072-3 1990 A mean sodium supplement of 2.2 mmol/kg per day (range 0.5-4.9), double the amount provided with feeds, was required to maintain plasma sodium concentration and plasma renin activity (PRA) in the normal range for age. Sodium 7-13 renin Homo sapiens 168-173 1977841-0 1990 Effect of sodium depletion on active renin, inactive renin and prekallikrein in plasma and urinary kallikrein excretion in glomerulonephritic patients. Sodium 10-16 renin Homo sapiens 37-42 2222965-3 1990 The metabolic set-point of these linked renin and calcium hormone systems, which serve to transduce environmental dietary mineral signals at the cellular level, determines the blood pressure consequences of sodium and calcium loading and/or restriction, and helps to explain the heterogeneous and seemingly inconsistent effects of these dietary maneuvers on blood pressure. Sodium 207-213 renin Homo sapiens 40-45 2379945-6 1990 Similarly, sodium restriction caused a 168% elevation of renal renin secretion (p less than 0.05). Sodium 11-17 renin Homo sapiens 63-68 2197881-1 1990 This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Sodium 42-48 renin Homo sapiens 141-146 2197881-1 1990 This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Sodium 42-48 renin Homo sapiens 222-227 2147304-7 1990 For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system. Sodium 162-168 renin Homo sapiens 179-184 2188754-10 1990 Moreover, renin response to sodium depletion appears to be an attribute that additionally characterizes individual hypertensive patients. Sodium 28-34 renin Homo sapiens 10-15 1977841-0 1990 Effect of sodium depletion on active renin, inactive renin and prekallikrein in plasma and urinary kallikrein excretion in glomerulonephritic patients. Sodium 10-16 renin Homo sapiens 53-58 2318519-3 1990 Renin-angiotensin system activation was evident within 24 hours after sodium intake was restricted. Sodium 70-76 renin Homo sapiens 0-5 2187635-10 1990 These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon"s syndrome, leading to volume expansion and suppression of renin and aldosterone. Sodium 45-51 renin Homo sapiens 162-167 2180817-9 1990 Similarly, a low sodium diet, which led to a slow increase in renal renin content, provoked large oscillations with high initial levels. Sodium 17-23 renin Homo sapiens 68-73 2251209-3 1990 Since it was not possible to establish a correlation between plasma renin activity and albumin level, as well as between this activity and aldosterone level, and aldosterone level and sodium excretion it may be surmised that the renin-angiotensin-aldosterone system has no decisive role in the pathogenesis of the nephrotic syndrome. Sodium 184-190 renin Homo sapiens 229-234 2198366-0 1990 [Effect of renin inhibitor (ES-1005) on expression of the kidney renin gene in sodium-depleted marmosets]. Sodium 79-85 renin Homo sapiens 11-16 2198366-0 1990 [Effect of renin inhibitor (ES-1005) on expression of the kidney renin gene in sodium-depleted marmosets]. Sodium 79-85 renin Homo sapiens 65-70 2160342-4 1990 Renin was responsive to posture, low sodium diet, saline infusion and frusemide, but relatively unresponsive to raising or lowering circulating levels of angiotensin II. Sodium 37-43 renin Homo sapiens 0-5 2187635-11 1990 Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities. Sodium 15-21 renin Homo sapiens 80-85 2284186-4 1990 Hyperactivity of the renin-aldosterone system determines the newborns" proneness to liquid and sodium retention. Sodium 95-101 renin Homo sapiens 21-26 2156654-7 1990 Plasma aldosterone and plasma renin activity increased during the sodium-depleted period but only plasma renin activity was significantly correlated with fractional excretion of filtered sodium. Sodium 187-193 renin Homo sapiens 105-110 2159502-8 1990 In both hypertensives and controls, plasma concentrations of active renin, angiotensin II and aldosterone decreased with increasing sodium intake, arginine vasopressin did not change, and atrial natriuretic factor and cyclic GMP increased. Sodium 132-138 renin Homo sapiens 68-73 2186360-0 1990 Stimulation of renin synthesis in the hydronephrotic kidney during sodium depletion. Sodium 67-73 renin Homo sapiens 15-20 2405233-8 1990 The results show that Bio-GH-induced retention of sodium involves the activation of the renin-angiotensin system. Sodium 50-56 renin Homo sapiens 88-93 1982809-2 1990 We have examined the relationship between the plasma renin level and serum sodium concentration in our CAPD patients. Sodium 75-81 renin Homo sapiens 53-58 1982809-4 1990 In forty-one patients a statistically significant inverse correlation between serum sodium and plasma renin levels was demonstrated. Sodium 84-90 renin Homo sapiens 102-107 1708025-9 1990 Sodium-dependent suppression of renin, angiotension II, aldosterone, and plasma catecholamines was comparable between the two groups. Sodium 0-6 renin Homo sapiens 32-37 2074437-7 1990 A sodium and water loss due to inhibition of tubular reabsorption leads to an increase in renin activity and aldosterone concentration in the plasma as seen typically with diuretics. Sodium 2-8 renin Homo sapiens 90-95 2154103-9 1990 This drop in plasma renin activity and aldosterone by 7 days post partum, in contrast with the unchanged high values of atrial natriuretic factor, may contribute to negative sodium balance after delivery. Sodium 174-180 renin Homo sapiens 20-25 2110866-5 1990 Oral administration of ES 6864 at 3 mg/kg to conscious, sodium-depleted marmosets inhibited plasma renin activity (PRA) more than 80% after 1 h. Sodium 56-62 renin Homo sapiens 99-104 2161301-5 1990 The results indicate that enhanced beta-adrenergic receptor function does accompany sympathetic activation during sodium restriction and converting enzyme inhibition and further support studies showing that the renin-angiotensin system plays the dominant role in blood pressure regulation in the sodium depleted state. Sodium 296-302 renin Homo sapiens 211-216 1706037-0 1990 Phosphate as a factor in sodium sensitivity in normal and high renin hypertension. Sodium 25-31 renin Homo sapiens 63-68 1706037-3 1990 The response of mean arterial pressure to sodium repletion was directly correlated to the response of plasma renin activity (r = 0.540, p = 0.004) and inversely related to the percent response of serum PO4 concentrations. Sodium 42-48 renin Homo sapiens 109-114 2137185-7 1990 In this regard, activation of the renin-angiotensin system locally reduces blood flow in the papilla which may be necessary before sodium retention is fully expressed in salt retaining states. Sodium 131-137 renin Homo sapiens 34-39 34967126-1 2022 This study aimed to evaluate the blood pressure (BP) lowing effect of low-sodium (LS) salt substitution and how the effect influenced by plasma renin concentration (PRC) on middle-aged and elderly hypertensive patients. Sodium 74-80 renin Homo sapiens 144-149 33778438-0 2021 Low sodium intake increases plasma renin activity. Sodium 4-10 renin Homo sapiens 35-40 35414109-1 2022 Supressed plasma renin in patients with primary hypertension is thought to be an indirect marker of sodium-induced volume expansion which is associated with more severe hypertension and hypertension-mediated organ damage. Sodium 100-106 renin Homo sapiens 17-22 34499251-3 2022 Our objective was to investigate if plasma renin activity and serum aldosterone are associated with urine sodium and potassium in youth referred for hypertensive disorders. Sodium 106-112 renin Homo sapiens 43-48 34499251-6 2022 We used multivariable generalized linear models to estimate the associations of renin and aldosterone with urine sodium and potassium. Sodium 113-119 renin Homo sapiens 80-85 35414109-10 2022 These results suggests that sodium retention in hypertension characterised by a low-renin state is associated with cell membrane damage reflected by eGCSS. Sodium 28-34 renin Homo sapiens 84-89 35620081-12 2022 Higher plasma total renin remained significantly associated with lower sodium output per doubling of diuretic dose (beta = -0.41 (-0.76, -0.059) per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower fractional excretion of sodium per doubling of diuretic dose (beta = -0.48 (-0.83, -0.14) and beta = -0.51 (-0.95, -0.08), respectively) in adjusted models. Sodium 71-77 renin Homo sapiens 20-25 35620081-12 2022 Higher plasma total renin remained significantly associated with lower sodium output per doubling of diuretic dose (beta = -0.41 (-0.76, -0.059) per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower fractional excretion of sodium per doubling of diuretic dose (beta = -0.48 (-0.83, -0.14) and beta = -0.51 (-0.95, -0.08), respectively) in adjusted models. Sodium 279-285 renin Homo sapiens 20-25 2532579-11 1989 Renal vein plasma renin activity increased by 56% with sodium restriction (P less than 0.01), whereas arterial ANP concentrations fell by 39% (P less than 0.05). Sodium 55-61 renin Homo sapiens 18-23 35475027-8 2022 Following oral sodium suppression, the aldosterone-to-renin ratio was 4-fold higher using immunoassay (27.2 (19.7, 62.4) vs 6.4 (3.5, 19.1) ng/dL per ng/mL/hour; P < .001). Sodium 15-21 renin Homo sapiens 54-59 2677101-6 1989 Supine plasma renin activity and plasma aldosterone were significantly lower during the high sodium diet. Sodium 93-99 renin Homo sapiens 14-19 2533223-0 1989 Impact of acute and chronic sodium loading on atrial natriuretic peptide and renin in man. Sodium 28-34 renin Homo sapiens 77-82 2533223-1 1989 The relationship between the renin-angiotensin system and the atrial natriuretic peptide and its contributions to the control of sodium balance is not clarified. Sodium 129-135 renin Homo sapiens 29-34 2512459-3 1989 The release of renin is followed by an increase in angiotensin II in the renal interstitium, which is responsible for adjusting the vascular tone of the efferent arterioles and vasa recta and for stimulating proximal tubular reabsorption of sodium. Sodium 241-247 renin Homo sapiens 15-20 2757896-2 1989 The renin-angiotensin-aldosterone-system is important for the maintenance of sodium balance in man. Sodium 77-83 renin Homo sapiens 4-9 2667598-0 1989 Pharmacological investigations of a new renin inhibitor in normal sodium-unrestricted volunteers. Sodium 66-72 renin Homo sapiens 40-45 2660287-7 1989 We speculate that normotensive subjects with low plasma renin activity present significant changes in the relationship between the renin-angiotensin-aldosterone system and sodium and calcium levels, and that this group is at risk for hypertension. Sodium 172-178 renin Homo sapiens 56-61 2660287-7 1989 We speculate that normotensive subjects with low plasma renin activity present significant changes in the relationship between the renin-angiotensin-aldosterone system and sodium and calcium levels, and that this group is at risk for hypertension. Sodium 172-178 renin Homo sapiens 131-136 2525347-5 1989 This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake. Sodium 112-118 renin Homo sapiens 65-70 2525347-5 1989 This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake. Sodium 212-218 renin Homo sapiens 65-70 2645917-0 1989 Blood pressure and serum calcium responses to altered sodium intake in high renin hypertension. Sodium 54-60 renin Homo sapiens 76-81 2490815-8 1989 The second, sodium-volume-related vasoconstriction, is marked by a reciprocally subnormal renin level and involves abnormal sodium retention and calcium transport. Sodium 12-18 renin Homo sapiens 90-95 2547039-2 1989 After acute intravenous administration to normotensive sodium-depleted marmosets, renin inhibitors of different structural types induced a maximum hypotensive response of a magnitude similar to that induced after angiotensin converting enzyme (ACE) inhibition. Sodium 55-61 renin Homo sapiens 82-87 2645917-1 1989 Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Sodium 49-55 renin Homo sapiens 19-24 2645917-1 1989 Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Sodium 129-135 renin Homo sapiens 19-24 2645917-6 1989 The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium. Sodium 41-47 renin Homo sapiens 63-68 2645917-6 1989 The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium. Sodium 41-47 renin Homo sapiens 161-166 2526071-2 1989 During chronic sodium loading, which increased mean body weight by 1.5 kg and markedly reduced plasma renin and aldosterone levels, plasma IR-ANP increased from 21 +/- 3 to 36 +/- 7 pmol/l (P less than 0.02). Sodium 15-21 renin Homo sapiens 102-107 2678894-3 1989 The variables threshold pressure and slope of the "renal baroreceptor"--mechanism of renin release serve different physiological functions: changes in slope (sensitivity) counteract short term changes in sodium balance whereas threshold pressure ensures a minimal systemic blood pressure associated with normal glomerular filtration. Sodium 204-210 renin Homo sapiens 85-90 2646216-0 1989 Renin regulation in type II diabetes mellitus: influence of dietary sodium. Sodium 68-74 renin Homo sapiens 0-5 2646216-10 1989 Inactive renin levels changed in a similar direction and magnitude as PRA in response to sodium intake and posture in the three study groups. Sodium 89-95 renin Homo sapiens 9-14 2708819-2 1989 The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. Sodium 4-10 renin Homo sapiens 154-159 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 15-20 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2654438-4 1989 Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Sodium 59-65 renin Homo sapiens 154-159 2654438-4 1989 Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Sodium 59-65 renin Homo sapiens 197-202 2576635-2 1989 Six NHS, acting in CHF, have presently been identified: three of them induce vasoconstriction and sodium retention (sympathetic nervous systems, renin-angiotensin-aldosterone system and arginine-vasopressine system); the remaining three offset or balance the former ones, acting, therefore as "counterregulators" (prostaglandins--PGE2 and PGI2--, dopaminergic system and atrial natriuretic factor). Sodium 98-104 renin Homo sapiens 145-150 2643968-8 1989 In contrast, plasma renin activity was greater in sickle cell patients at all levels of sodium intake in both supine and upright positions. Sodium 88-94 renin Homo sapiens 20-25 2474103-2 1989 Homeostatic mechanisms, including activation of the renin-aldosterone system, may counteract the effects of sodium restriction. Sodium 108-114 renin Homo sapiens 52-57 2699788-0 1989 [Effect of sodium depletion on the renin-angiotensin-aldosterone system and prostaglandins in patients with insulin-dependent diabetes mellitus]. Sodium 11-17 renin Homo sapiens 35-40 2483424-6 1989 The synthesis of renin is initiated when the cAMP concentration increases under the influence of hormones (parathyroid hormone, catecholamines), of mediators (e.g., prostanoids), or of changes in composition of tubular fluid (in sodium, chlorine, or calcium) detected by the macula densa. Sodium 229-235 renin Homo sapiens 17-22 2474096-9 1989 This suggests that local angiotensin concentrations in the vascular and renin tissues may be more important in determining sodium and water excretion. Sodium 123-129 renin Homo sapiens 72-77 2663759-4 1989 Transplanted kidneys show a preserved reaction pattern of renin secretion to sodium deprivation and upright position. Sodium 77-83 renin Homo sapiens 58-63 2701770-3 1989 Renin and aldosterone levels significantly increased in group C. A significant correlation was observed between plasma aldosterone concentration and urinary sodium excretion, and between plasma renin activity and aldosterone levels. Sodium 157-163 renin Homo sapiens 0-5 2977171-7 1988 These findings are consistent with a renal tubular avidity for sodium, leading to volume expansion, suppression of renin, and, depending on dietary sodium intake, hypertension. Sodium 63-69 renin Homo sapiens 115-120 3058795-8 1988 These adaptive responses provide a basis for the observation that the inhibition of renin activity with converting enzyme inhibitors in essential hypertension increases renal blood flow and sodium excretion. Sodium 190-196 renin Homo sapiens 84-89 3071591-6 1988 The circulating renin-angiotensin system was stimulated by sodium depletion, and the cerebrospinal fluid concentration of Ang II also increased significantly. Sodium 59-65 renin Homo sapiens 16-21 3071591-7 1988 Sodium depletion may stimulate the brain Ang-II forming system, as it does the circulating renin-angiotensin system. Sodium 0-6 renin Homo sapiens 91-96 3071599-0 1988 Norepinephrine and calcium responses to altered sodium intake in modulating and non-modulating high-renin hypertension. Sodium 48-54 renin Homo sapiens 100-105 3071599-1 1988 Sodium sensitivity in subjects with high-renin hypertension has been associated with non-modulation of cardiovascular and biochemical responses to alteration in sodium intake. Sodium 0-6 renin Homo sapiens 41-46 3071599-2 1988 Using the percentage suppression of plasma renin activity in response to an increase in dietary sodium intake, high-renin hypertensive subjects were categorized in two groups. Sodium 96-102 renin Homo sapiens 43-48 3071599-3 1988 In association with the increase in sodium intake, modulators showed greater than 58% suppression of plasma renin activity, and significant reductions in mean arterial pressure, plasma aldosterone, norepinephrine and serum calcium concentration. Sodium 36-42 renin Homo sapiens 108-113 3071599-5 1988 The blood pressure response to an increase in dietary sodium intake may be a composite of responses of the renin-angiotensin-aldosterone axis, the adrenergic nervous system and calcium regulatory system. Sodium 54-60 renin Homo sapiens 107-112 3154627-4 1988 A low-sodium diet or a high-potassium diet, or nephrectomy markedly increases the adrenal renin concentration in the zona glomerulosa cells without any effect on the fasciculata-medullary cells. Sodium 6-12 renin Homo sapiens 90-95 3058795-9 1988 They also explain why converting enzyme inhibitors can effectively reduce blood pressure, even when renin levels are not absolutely elevated, since any circulating renin imposed upon the adapting hypernatriuretic nephrons inappropriately impairs their sodium excretion. Sodium 252-258 renin Homo sapiens 164-169 3058795-12 1988 The net effect of this uncoordinated response is to shift total renal function so that systemic arterial hypertension is sustained by abnormal sodium retention for the inappropriately high plasma renin level, or vice versa. Sodium 143-149 renin Homo sapiens 196-201 3046266-3 1988 Because of changes in the renin-aldosterone system, the elderly may have problems maintaining sodium and potassium balance. Sodium 94-100 renin Homo sapiens 26-31 2850819-1 1988 In a previous paper, we showed that during a long-term, moderate restriction in sodium intake, sympathetic nervous system activity was only transiently stimulated, whereas a sustained rise of plasma renin activity occurred. Sodium 80-86 renin Homo sapiens 199-204 3054233-8 1988 Low-renin vasoconstriction is correctable by sodium depletion or by calcium channel or alpha adrenergic blockade. Sodium 45-51 renin Homo sapiens 4-9 3284356-5 1988 Sodium-sensitive individuals were characterized by significantly increased forearm vascular resistance and decreased plasma renin activity and aldosterone concentration. Sodium 0-6 renin Homo sapiens 124-129 3294177-7 1988 In patients with essential hypertension, intracellular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r = -0.66, p less than 0.001; r = -0.60, p less than 0.001, plasma norepinephrine concentration. Sodium 55-61 renin Homo sapiens 133-138 3294177-8 1988 These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity. Sodium 84-90 renin Homo sapiens 241-246 3294177-8 1988 These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity. Sodium 201-207 renin Homo sapiens 241-246 3286047-9 1988 They also show a blunted rate of renin suppression after a sodium load, although plasma renin activity falls to the same low level at steady state. Sodium 59-65 renin Homo sapiens 33-38 3389028-4 1988 This fall appears to be mediated in part by a diminished renin response to the sodium restriction as blood pressure becomes more severe. Sodium 79-85 renin Homo sapiens 57-62 2851654-7 1988 Plasma renin was increased by enalapril and lowered by increased sodium intake. Sodium 65-71 renin Homo sapiens 7-12 2975458-8 1988 These data confirm that atrial natriuretic peptide inhibits renin secretion in a dose-related manner and suggest that this action of the peptide is modified by both the baseline sodium status and renal function of the recipient. Sodium 178-184 renin Homo sapiens 60-65 2975463-4 1988 Plasma renin activity was related to 24-hour urinary sodium excretion. Sodium 53-59 renin Homo sapiens 7-12 2967239-4 1988 Sodium loading increased resting supine plasma IR-ANP (P less than 0.037) and suppressed plasma renin and aldosterone, including the renin-aldosterone response to exercise. Sodium 0-6 renin Homo sapiens 96-101 2967239-4 1988 Sodium loading increased resting supine plasma IR-ANP (P less than 0.037) and suppressed plasma renin and aldosterone, including the renin-aldosterone response to exercise. Sodium 0-6 renin Homo sapiens 133-138 3283072-7 1988 In addition, patients of both groups showed normal response of the renin-aldosterone system following diuretic and dietary induced sodium and volume depletion. Sodium 131-137 renin Homo sapiens 67-72 2900130-1 1988 In this paper the different aspects of the role played by alpha-adrenoceptors in the control of renin secretion from the juxtaglomerular apparatus and renal sodium and water reabsorption, and the effects of alpha-adrenoceptor antagonists on systemic haemodynamics, will be investigated. Sodium 157-163 renin Homo sapiens 96-101 3076742-0 1988 Plasma renin activity in patients with sodium-sensitive and sodium-resistant symptomatic arterial hypertension. Sodium 39-45 renin Homo sapiens 7-12 3076742-0 1988 Plasma renin activity in patients with sodium-sensitive and sodium-resistant symptomatic arterial hypertension. Sodium 60-66 renin Homo sapiens 7-12 3072177-2 1988 The first is renin-independent, requires antecedent sodium retention, and appears related to abnormal membrane transport of calcium. Sodium 52-58 renin Homo sapiens 13-18 2824371-0 1987 Humoral sodium transport inhibitor in acute volume expansion and low renin hypertension. Sodium 8-14 renin Homo sapiens 69-74 3287122-0 1988 [Plasma renin activity in relation to sodium excretion. Sodium 38-44 renin Homo sapiens 8-13 2977818-1 1988 Atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone system are important regulatory hormones in sodium homeostasis. Sodium 115-121 renin Homo sapiens 41-46 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 11-17 renin Homo sapiens 103-108 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 145-151 renin Homo sapiens 199-204 2970180-3 1988 Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Sodium 200-206 renin Homo sapiens 182-187 3326697-3 1987 Evidence is presented that the renin-angiotensin-aldosterone system and the adrenergic nervous system are important determinants of the blood pressure response to sodium depletion and sodium loading, respectively. Sodium 163-169 renin Homo sapiens 31-36 3326697-3 1987 Evidence is presented that the renin-angiotensin-aldosterone system and the adrenergic nervous system are important determinants of the blood pressure response to sodium depletion and sodium loading, respectively. Sodium 184-190 renin Homo sapiens 31-36 3326859-0 1987 Relationship between plasma renin activity and distal nephron sodium delivery and reabsorption in man. Sodium 62-68 renin Homo sapiens 28-33 3326859-1 1987 The relationship between plasma renin activity and distal tubular sodium delivery and reabsorption was examined in man. Sodium 66-72 renin Homo sapiens 32-37 3326859-3 1987 The maximal water diuresis method and the lithium clearance method both showed a negative correlation between plasma renin activity and distal sodium delivery and reabsorption. Sodium 143-149 renin Homo sapiens 117-122 3037881-4 1987 These results suggest that the increased plasma levels of atrial natriuretic peptide, which appear to be associated with an increase in plasma renin activity and with hepatic dysfunction, may participate in maintaining homeostasis of sodium and fluid volume in patients with chronic liver disease. Sodium 234-240 renin Homo sapiens 143-148 3314453-3 1987 The first mechanism is renin independent, requires antecedent sodium retention and appears related to abnormal membrane transport of calcium. Sodium 62-68 renin Homo sapiens 23-28 3314453-4 1987 This vasoconstriction is identified by low plasma renin and ionized calcium and is correctable by sodium depletion or calcium channel or alpha blockade. Sodium 98-104 renin Homo sapiens 50-55 3308701-1 1987 We have reported that 50% of subjects with normal renin essential hypertension have both delayed suppression of the renin-angiotensin-aldosterone axis following sodium infusion and a delayed rate of excretion of an acute salt load. Sodium 161-167 renin Homo sapiens 116-121 3480991-0 1987 Sodium sensitivity and resistance of blood pressure: the role of the kidney and the renin-aldosterone axis. Sodium 0-6 renin Homo sapiens 84-89 3078193-0 1987 [Plasma renin activity in patients with sodium-responsive and unresponsive essential hypertension]. Sodium 40-46 renin Homo sapiens 8-13 3300326-4 1987 Upright plasma renin activity was suppressed in cyclosporine-treated patients (cyclosporine 2.9 +/- 0.9, azathioprine 4.7 +/- 0.9, renal insufficiency 5.2 +/- 1.9 ng/ml/hour) but could be stimulated by a four-day period of dietary sodium restriction and diuretic administration (cyclosporine 15.8 +/- 4.4 ng/ml/hour). Sodium 231-237 renin Homo sapiens 15-20 3323041-0 1987 Urinary sodium & plasma renin activity following renal transplantation. Sodium 8-14 renin Homo sapiens 28-33 3300326-7 1987 It is concluded that suppression of plasma renin activity by cyclosporine is physiologic and may reflect expansion of extracellular fluid volume, which can be reversed by sodium depletion. Sodium 171-177 renin Homo sapiens 43-48 2882875-3 1987 When sodium intake is restricted or a diuretic is used, the reactive increase in plasma renin activity makes a substantial contribution to limiting the decrease in blood pressure. Sodium 5-11 renin Homo sapiens 88-93 3115635-2 1987 During an in-patient metabolic balance study she required 1.0 mg fludrocortisone daily and dietary sodium supplementation to make plasma renin activity and serum potassium normal, and to abolish postural hypotension. Sodium 99-105 renin Homo sapiens 137-142 3035964-2 1987 Plasma renin activity, its response to sodium depletion, and the renal vein renin ratio during sodium depletion were greater in unilateral than in bilateral stenosis. Sodium 95-101 renin Homo sapiens 76-81 3035964-3 1987 A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Sodium 69-75 renin Homo sapiens 129-134 3035964-3 1987 A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Sodium 69-75 renin Homo sapiens 168-173 3301353-4 1987 This fall appears to be mediated in part by a diminished renin response to the sodium restriction as blood pressure becomes more severe. Sodium 79-85 renin Homo sapiens 57-62 3552505-4 1987 Using univariate analysis, all the patients with poor sodium excretion had abnormally high levels of plasma renin activity, plasma aldosterone, and arginine vasopressin. Sodium 54-60 renin Homo sapiens 108-113 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 91-96 2882685-7 1987 As in humans, active and inactive plasma renin increased during sodium depletion and inactive renin increased during beta-adrenergic blockade, while active renin decreased. Sodium 64-70 renin Homo sapiens 41-46 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 62-67 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 91-96 3319647-4 1987 Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). Sodium 79-85 renin Homo sapiens 5-10 3580257-0 1987 The importance of the response of the renin-angiotensin system in determining blood pressure changes with sodium restriction. Sodium 106-112 renin Homo sapiens 38-43 3580257-3 1987 This lack of response of blood pressure to sodium restriction appears to be due, at least in part, to a reactive rise in renin and angiotensin II. Sodium 43-49 renin Homo sapiens 121-145 3580257-5 1987 With sodium restriction there is less of a rise in renin and angiotensin II compared with normotensive subjects and patients have a greater fall in blood pressure compared with normotensive subjects but the effect is less in mild compared to severe hypertension. Sodium 5-11 renin Homo sapiens 51-56 3549504-6 1987 We confirmed the inverse correlation between serum sodium and serum renin. Sodium 51-57 renin Homo sapiens 68-73 2948754-3 1987 Plasma renin activity and aldosterone decreased significantly with increasing sodium intake whereas plasma vasopressin was highest on the high sodium intake. Sodium 78-84 renin Homo sapiens 7-12 3532893-6 1986 Calcium-regulating hormones and the renin-aldosterone system may coordinately mediate the blood pressure effects of differing dietary calcium and sodium intakes at the cellular level by altering cellular handling of monovalent and divalent ions. Sodium 146-152 renin Homo sapiens 36-41 3553473-0 1986 Natriuresis and the renin axis in sodium-sensitive man. Sodium 34-40 renin Homo sapiens 20-25 3553473-3 1986 Sodium-sensitive individuals had lower renin values than those who were resistant to sodium. Sodium 0-6 renin Homo sapiens 39-44 3553473-5 1986 Sodium-sensitive subjects exhibited greater aldosterone responses to renin stimulation after volume depletion than resistant subjects. Sodium 0-6 renin Homo sapiens 69-74 3553473-6 1986 Sodium sensitivity is associated with exaggerated natriuresis as well as tighter coupling between renin and aldosterone. Sodium 0-6 renin Homo sapiens 98-103 3126454-0 1987 The renin-angiotensin-aldosterone system during haemodialysis with acetate or bicarbonate at different dialysate sodium concentrations. Sodium 113-119 renin Homo sapiens 4-9 3126454-3 1987 At lower dialysate sodium concentrations, plasma renin activity (acetate dialysis and bicarbonate dialysis) and aldosterone concentration (only acetate dialysis) were higher than they were at higher dialysate sodium concentrations. Sodium 19-25 renin Homo sapiens 49-54 2944381-6 1986 The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Sodium 222-228 renin Homo sapiens 4-9 3021923-2 1986 Abnormally high ambulatory plasma renin activity was seen in 14 of 19 patients with 24-hour urine sodium excretion greater than 50 mEq. Sodium 98-104 renin Homo sapiens 34-39 3795712-5 1986 Changes in renin-angiotensin-aldosterone activity showed close correlation with changes in sodium balance. Sodium 91-97 renin Homo sapiens 11-16 2947978-5 1986 Toward the other end of the spectrum, revealed by the finding of low plasma renin, a sodium-volume-induced form of vasoconstriction operates. Sodium 85-91 renin Homo sapiens 76-81 2943356-4 1986 Concentrations of both atrial natriuretic peptide and renin showed significant inverse relations with serum sodium concentrations. Sodium 108-114 renin Homo sapiens 54-59 3531301-7 1986 Fetal plasma renin activity was inversely related to fetal plasma sodium levels (P less than 0.01). Sodium 66-72 renin Homo sapiens 13-18 3531413-4 1986 Moderate reduction of sodium intake is additive to the effect of blood-pressure-lowering drugs, particularly those that block the renin-angiotensin system such as beta-blockers and converting enzyme inhibitors. Sodium 22-28 renin Homo sapiens 130-135 3522418-8 1986 In both groups sodium-sensitive individuals were significantly older (p less than 0.001) and had lower baseline renin values than sodium-resistant subjects. Sodium 15-21 renin Homo sapiens 112-117 3518053-7 1986 Thus, in cirrhotic alcoholic patients with ascites the determination of daily urinary sodium excretion, which is inversely related to the activity of the renin-angiotensin system, provides a useful prognostic index for the response to salt restriction and longterm survival. Sodium 86-92 renin Homo sapiens 154-159 2941538-2 1986 In this endocrine control, the renin axis provides the primary defence against sodium volume depletion and hypotension while atrial hormone plays an increasingly active counter-role for coping with situations that involve a sodium-volume surfeit or rising blood volume or blood pressure levels. Sodium 79-85 renin Homo sapiens 31-36 3517066-5 1986 Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. Sodium 139-145 renin Homo sapiens 5-10 3517066-6 1986 For both diets, plasma renin and urinary aldosterone excretion were correlated with urinary sodium excretion (r = -0.768, r = -0.726, respectively; P less than 0.005). Sodium 92-98 renin Homo sapiens 23-28 2943142-2 1986 Renin release may result from one of several different stimuli: renal tubular sodium delivery and sensing by the macula densa, sympathetic nervous system activity, and baroreceptor to changes in renal blood flow. Sodium 78-84 renin Homo sapiens 0-5 3519007-1 1986 To clarify age-related changes in the plasma renin activity (PRA)-aldosterone (ALDO) system in relation to urinary sodium (Na) excretion in pseudohypoaldosteronism type I (PHA), we followed a patient with PHA serially by measuring the hormonal balance and urinary electrolyte excretion for 5 years. Sodium 115-121 renin Homo sapiens 45-50 3002660-6 1986 This interaction between serum sodium concentration, drug treatment, and long-term outcome suggests that the renin-angiotensin system may exert a deleterious effect on the survival of some patients with chronic heart failure, which can be antagonized by converting enzyme inhibition, and provides a clinical counterpart for the similar prognostic role that has been postulated for angiotensin II in experimental preparations of heart failure. Sodium 31-37 renin Homo sapiens 109-114 3524920-5 1986 The basic abnormality is excessive renal sodium retention, leading to chronic suppression of renin and aldosterone; the latter is then hyporesponsive to the hyperkalaemic stimulus. Sodium 41-47 renin Homo sapiens 93-98 3514728-6 1986 Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Sodium 117-123 renin Homo sapiens 17-22 2943142-9 1986 In an analysis of the factors that may result in renin release, tubular delivery of sodium to the macula densa may emerge as the most important regulator of renin release. Sodium 84-90 renin Homo sapiens 49-54 2943142-9 1986 In an analysis of the factors that may result in renin release, tubular delivery of sodium to the macula densa may emerge as the most important regulator of renin release. Sodium 84-90 renin Homo sapiens 157-162 2952486-17 1986 However, since peripheral resistance was not changed, another non-renin, sodium-related mechanism must take over to sustain increased arterial constriction. Sodium 73-79 renin Homo sapiens 66-71 3535395-4 1986 Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). Sodium 54-60 renin Homo sapiens 7-12 3530563-9 1986 Patients who responded to sodium restriction had a lower initial renin value than other patients. Sodium 26-32 renin Homo sapiens 65-70 3530563-10 1986 This study emphasises the importance of the interaction between sodium, potassium and renin in the determination of blood pressure levels. Sodium 64-70 renin Homo sapiens 86-91 3716879-6 1986 The decrease in urinary sodium excretion was associated with increases in plasma renin activity and urinary aldosterone excretion, while a sympathetic nervous natriuretic index (urinary dopamine to noradrenaline excretion ratio) decreased. Sodium 24-30 renin Homo sapiens 81-86 3716879-11 1986 We conclude that moderate sodium restriction lowered the blood pressure and affected the renin-aldosterone and sympathetic nervous system to retain sodium which might explain the constancy of the plasma volume. Sodium 26-32 renin Homo sapiens 89-94 3716879-11 1986 We conclude that moderate sodium restriction lowered the blood pressure and affected the renin-aldosterone and sympathetic nervous system to retain sodium which might explain the constancy of the plasma volume. Sodium 148-154 renin Homo sapiens 89-94 2939792-7 1986 In this construction the renin system acts primarily to defend sodium balance and blood pressure, with the atrial hormone playing an increasingly active counterpart in situations involving sodium-volume surfeit and/or high blood pressure. Sodium 63-69 renin Homo sapiens 25-30 2425102-2 1986 Recently, we have shown that aprotinin, a kallikrein inhibitor, inhibits the stimulation of plasma renin activity (PRA) by either furosemide or a low sodium diet. Sodium 150-156 renin Homo sapiens 99-104 3957560-2 1986 Plasma renin activity was very high (median 29.0 ng/ml/hr) at admission, decreased after equilibration with a normal sodium diet (9.9 ng/ml/hr) and was negatively correlated with urinary sodium excretion. Sodium 117-123 renin Homo sapiens 7-12 3957560-2 1986 Plasma renin activity was very high (median 29.0 ng/ml/hr) at admission, decreased after equilibration with a normal sodium diet (9.9 ng/ml/hr) and was negatively correlated with urinary sodium excretion. Sodium 187-193 renin Homo sapiens 7-12 2422494-4 1986 Because of the activation of the renin-angiotensin system, angiotensin-mediated vasoconstriction and aldosterone-mediated sodium retention can be suppressed and, in some individuals, completely blocked by converting enzyme inhibitors. Sodium 122-128 renin Homo sapiens 33-38 2425102-9 1986 These results suggest that both renal kallikrein and prostaglandins play an important role in the control of renin release under sodium depletion. Sodium 129-135 renin Homo sapiens 109-114 3635150-5 1986 The principal effectors of renal sodium retention and vasoconstriction are stimulation of the renin-angiotensin-aldosterone axis and augmentation of renal sympathetic nerve activity. Sodium 33-39 renin Homo sapiens 94-99 2866706-3 1985 When sodium intake is restricted or a diuretic is used, the reactive increase in plasma renin activity makes a substantial contribution to limiting the blood pressure fall. Sodium 5-11 renin Homo sapiens 88-93 3765573-6 1986 The changes in plasma sodium of the subgroups of patients with essential hypertension are accompanied by certain deviations in hemodynamics, in plasma aldosterone and in plasma renin activity. Sodium 22-28 renin Homo sapiens 177-182 2866707-1 1985 The renin-angiotensin-aldosterone system regulates blood pressure and volume homeostasis in addition to sodium and potassium metabolism, and may be linked to divalent cation metabolism as well as hypertensive disease. Sodium 104-110 renin Homo sapiens 4-9 3907374-7 1985 Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. Sodium 198-204 renin Homo sapiens 24-29 2856782-3 1985 We studied calcium metabolism in essential hypertension and used renin-sodium profiling, which reveals the biochemical heterogeneity of clinical hypertension. Sodium 71-77 renin Homo sapiens 65-70 2932646-1 1985 The renin-angiotensin-aldosterone axis exerts major control over sodium and potassium balance and arterial blood pressure. Sodium 65-71 renin Homo sapiens 4-9 2856729-7 1985 During sodium restriction, plasma renin activity and urinary aldosterone excretion significantly increased. Sodium 7-13 renin Homo sapiens 34-39 2932646-3 1985 In addition, changes in intrarenal physical factors cause changes in the supply of distal tubular sodium that, in turn, work to determine sodium and potassium excretion and to modulate the release of renal renin. Sodium 98-104 renin Homo sapiens 206-211 2932646-10 1985 In this construction the renin system primarily defends sodium balance and blood pressure, with the atrial hormone having an increasing counter-influence in situations involving high blood pressure or sodium surfeit. Sodium 56-62 renin Homo sapiens 25-30 2864856-1 1985 Relationship to blood pressure, renin-sodium profiles, and antihypertensive therapy. Sodium 38-44 renin Homo sapiens 32-37 2865701-3 1985 The high catecholamine values in cirrhotic patients and the activation of the renin angiotensin-aldosterone system suggest the use of beta-blockers to reduce sodium-water retention. Sodium 158-164 renin Homo sapiens 78-83 3897045-6 1985 In the patients, equilibrium after raised sodium intake was accompanied by a marked increase in blood pressure and blood volume, a moderate fall in plasma renin activity and levels of aldosterone and norepinephrine, and only little expansion of the interstitial space. Sodium 42-48 renin Homo sapiens 155-160 3897045-9 1985 In the normal volunteers, increasing the sodium intake from 20 to 1128 mEq/day evoked no consistent change in blood pressure but caused a comparable rise in blood volume, considerable suppression of plasma renin activity, aldosterone, and norepinephrine, and a much larger increase in interstitial volume. Sodium 41-47 renin Homo sapiens 206-211 3012004-6 1985 The log of the initial plasma renin activity correlated with the changes in blood pressure (r = 0.59, p less than 0.05) in effective renal plasma flow (r = 0.59, p less than 0.05) and in sodium excretion (r = 0.65, p less than 0.01). Sodium 187-193 renin Homo sapiens 30-35 4006354-4 1985 Sodium and potassium chloride supplementation lead to improved growth and strength, partial correction of his electrolyte abnormalities, and a decrease in markedly elevated plasma renin activity. Sodium 0-6 renin Homo sapiens 180-185 2992406-4 1985 Studies with these agents have clearly shown that the renin-angiotensin system plays an important role in the defense of body balance and blood pressure in hypovolemic state, including sodium deficiency and hemorrhage. Sodium 185-191 renin Homo sapiens 54-59 3901077-0 1985 The renin-angiotensin-aldosterone system in decompensated cirrhosis: its activity in relation to sodium balance. Sodium 97-103 renin Homo sapiens 4-9 3909580-7 1985 At this late stage of renal hypertension renin may play a contributory role.Thus, the primary abnormality in the chain of events leading eventually to hypertension is a renal inability to maintain a proper balance between sodium intake and output. Sodium 222-228 renin Homo sapiens 41-46 3911719-9 1985 Almost in every patient with a serum sodium concentration lower or equal 132 mmol/l the plasma renin activity was markedly elevated. Sodium 37-43 renin Homo sapiens 95-100 3894515-0 1985 Sodium restriction lowers high blood pressure through a decreased response of the renin system--direct evidence using saralasin. Sodium 0-6 renin Homo sapiens 82-87 3894515-4 1985 A highly significant negative correlation was found between the fall in blood pressure on sodium restriction and the change in blood pressure with saralasin (r = -0.52; P less than 0.005); this correlation was still significant when corrected for the severity of the hypertension (r = -0.41; P = 0.03) while it became non-significant if controlled for plasma renin activity on the low sodium diet (r = -033; NS). Sodium 90-96 renin Homo sapiens 359-364 3894515-5 1985 These results provide direct evidence that the fall in blood pressure which is seen on reducing sodium intake in many patients with essential hypertension is, at least in part, directly mediated by the reactivity of the renin angiotensin system. Sodium 96-102 renin Homo sapiens 220-225 3904334-0 1985 The sodium intake modifies the renin-aldosterone and blood pressure changes associated with moderately low energy diets. Sodium 4-10 renin Homo sapiens 31-36 3926508-0 1985 Active and acid-activable inactive renin during inhibition by indomethacin of prostaglandin synthesis in sodium-replete man. Sodium 105-111 renin Homo sapiens 35-40 2981464-1 1985 The renin-angiotension system is activated in many patients with congestive heart failure (CHF), resulting in angiotensin-mediated vasoconstriction and aldosterone-mediated sodium and water retention. Sodium 173-179 renin Homo sapiens 4-9 3911719-10 1985 Patients with normal serum sodium concentrations exhibited only slightly elevated plasma renin activity. Sodium 27-33 renin Homo sapiens 89-94 2412019-2 1985 The administration of saralasin or captopril and, in the near future, of renin inhibitors induces a fall in blood pressure that is variable from one subject to the other according to the sodium balance and the level of activation of the system. Sodium 187-193 renin Homo sapiens 73-78 3894477-1 1985 Eight normotensive obese subjects participated in an inpatient study designed to determine the effect of a constant sodium intake (150 mEq) on the renin-aldosterone axis during 12 weeks of weight reduction. Sodium 116-122 renin Homo sapiens 147-152 2983148-3 1985 Renin and aldosterone measurements showed that changes in the sodium and potassium excretion were produced by a lower activity of the renin-angiotensin-aldosterone system in the first 1.5 hour of hypokinesia. Sodium 62-68 renin Homo sapiens 0-5 2983148-3 1985 Renin and aldosterone measurements showed that changes in the sodium and potassium excretion were produced by a lower activity of the renin-angiotensin-aldosterone system in the first 1.5 hour of hypokinesia. Sodium 62-68 renin Homo sapiens 134-139 4050888-9 1985 The limited effect on blood pressure and the renin system of a marked sodium removal during salt subtraction suggests that sodium must still be present in excess in these patients. Sodium 70-76 renin Homo sapiens 45-50 2412009-4 1985 The action may be due to (a) a change in glomerular filtration rate and/or renal blood flow; (b) interference with renin release; (c) interference with aldosterone secretion and/or aldosterone action on distal tubule; (d) interference with adrenergic sodium handling; (e) a direct tubular action. Sodium 251-257 renin Homo sapiens 115-120 2412016-9 1985 The results of these comparative studies suggest that, in states of sodium depletion, the acute hypotensive effects of renin- or CE-inhibitors are entirely due to their interference with the renin-angiotensin system. Sodium 68-74 renin Homo sapiens 119-125 2412016-9 1985 The results of these comparative studies suggest that, in states of sodium depletion, the acute hypotensive effects of renin- or CE-inhibitors are entirely due to their interference with the renin-angiotensin system. Sodium 68-74 renin Homo sapiens 119-124 6391132-7 1984 The renin-angiotensin system is activated in these patients, in part to preserve sodium homeostasis. Sodium 81-87 renin Homo sapiens 4-9 3906991-4 1985 In patients with renal failure, diuresis also increased, however sodium excretion with urine dramatically reduced which was accompanied by inhibition of plasma renin activity. Sodium 65-71 renin Homo sapiens 160-165 6100873-6 1984 The renin-angiotensin system plays a role in the regulation of blood pressure levels in normal experimental animals and man--its importance depending on the state of sodium balance. Sodium 166-172 renin Homo sapiens 4-9 6746861-5 1984 Both assays gave almost identical results in normal subjects whereas in three different conditions characterized by a high renin level (severe hypertension plus low sodium diet, converting enzyme inhibition, and adrenal insufficiency) higher results were obtained by the direct assay. Sodium 165-171 renin Homo sapiens 123-128 6094854-0 1984 Effects of sodium, potassium, ACTH and nephrectomy on adrenal renin. Sodium 11-17 renin Homo sapiens 62-67 6598066-5 1984 This was attributed to thorough biochemical evaluation of the underlying metabolic state by measurement of renal potassium handling and by determining the responses of the renin-aldosterone axis to changes in sodium balance. Sodium 209-215 renin Homo sapiens 172-177 6394181-3 1984 The greatest fall in blood pressure with sodium restriction was seen in those patients with the least rise in renin. Sodium 41-47 renin Homo sapiens 110-115 6428366-1 1984 The renin-aldosterone system contributes to the regulation of arterial pressure and to the maintenance of sodium and potassium balance. Sodium 106-112 renin Homo sapiens 4-9 6202963-9 1984 A significant decrease in renal sodium and water excretion occurred only during administration of the highest dose of 50 mg t.i.d., when reduction in blood pressure was pronounced and there were reflex increases in plasma renin activity and plasma aldosterone. Sodium 32-38 renin Homo sapiens 222-227 6143083-8 1984 Responsiveness of the renin-angiotensin system may limit the fall in blood-pressure induced by sodium restriction. Sodium 95-101 renin Homo sapiens 22-27 6323565-4 1984 The changes in mean arterial pressure and left ventricular filling pressure seen with first doses of the drug varied linearly and inversely with the pretreatment serum sodium concentration (r = -0.58 and r = -0.53, respectively); this was likely related to the finding that, before administration of captopril, the serum sodium concentration varied linearly and inversely with the logarithm of the plasma renin activity (r = -0.78). Sodium 168-174 renin Homo sapiens 405-410 6199985-11 1984 In normotensive marmosets the renin-angiotensin system participates in the maintenance of blood pressure, to a degree depending on the state of sodium balance. Sodium 144-150 renin Homo sapiens 30-35 6368215-9 1984 Prolonged hypovolemic hypotension or sodium depletion increases renin levels. Sodium 37-43 renin Homo sapiens 64-69 6097382-4 1984 Plasma renin activity increased after ACTH infusion only on the lower sodium intake. Sodium 70-76 renin Homo sapiens 7-12 6372072-7 1984 Measurement of renin and aldosterone levels should be used for evaluation of the severity of a sodium deficiency. Sodium 95-101 renin Homo sapiens 15-20 6361570-5 1984 Individual serum sodium concentrations were inversely correlated with levels of prostaglandin E2 metabolites (r = -0.92, P less than 0.001) and plasma renin activity (r = -0.69, P less than 0.02). Sodium 17-23 renin Homo sapiens 151-156 6204138-6 1984 Pharmacologic interruption of the renin-angiotensin system is proving useful not only for blood pressure control in patients with hypertension but also because of its influence on the kidney in some or all of these conditions--at least in part attributable to restoration of more normal renal sodium handling. Sodium 293-299 renin Homo sapiens 34-39 6378223-0 1983 [Nyctohemeral values of plasma renin and aldosterone in relation to age, sex and sodium intake and posture]. Sodium 81-87 renin Homo sapiens 31-36 6371561-2 1984 Recent evidence has shown that many patients with the nephrotic syndrome have a normal or low plasma renin activity suggesting that there might be an intrarenal cause for their sodium retention. Sodium 177-183 renin Homo sapiens 101-106 6382488-0 1984 Expression of plasma renin activity in terms of urinary sodium excretion and posture in normal subjects on free sodium intake. Sodium 56-62 renin Homo sapiens 21-26 6382488-2 1984 Supine and upright plasma renin activities were then related to the 24-hour urinary sodium or the 2-hour urinary sodium excretion, measured in the morning after overnight fasting. Sodium 84-90 renin Homo sapiens 26-31 6382488-2 1984 Supine and upright plasma renin activities were then related to the 24-hour urinary sodium or the 2-hour urinary sodium excretion, measured in the morning after overnight fasting. Sodium 113-119 renin Homo sapiens 26-31 6196232-12 1983 Studies with monkeys show that a peptide renin inhibitors may cause hypotension after sodium depletion and normalize blood pressure in Goldblatt hypertension to the same degree as a converting-enzyme inhibitor. Sodium 86-92 renin Homo sapiens 41-46 6085835-9 1983 We have also found that plasma renin values in heart failure are dependent on sodium intake. Sodium 78-84 renin Homo sapiens 31-36 6345048-5 1983 The usual two- to three-fold rise in plasma renin activity and angiotensin II observed in normal subjects on assumption of the upright posture after ingestion of 200 mg of sodium/day failed to occur in the kininogen-deficient individual. Sodium 172-178 renin Homo sapiens 44-49 6400115-3 1983 At the same time there was attenuation of the expected increase in plasma renin activity appropriate for such a sodium loss. Sodium 112-118 renin Homo sapiens 74-79 6360917-0 1983 Renin-aldosterone axis in ethanol intoxication during sodium and fluid repletion versus depletion. Sodium 54-60 renin Homo sapiens 0-5 6360917-3 1983 In sodium-depleted subjects starting levels of plasma renin activity (PRA) and plasma aldosterone were increased as expected. Sodium 3-9 renin Homo sapiens 54-59 6354522-8 1983 On the low sodium intake, the enhanced PA response to MCP probably reflects both a direct adrenal effect and an indirect effect mediated via activation of the renin-angiotensin system. Sodium 11-17 renin Homo sapiens 159-164 6400108-2 1983 The renin-angiotensin system, renal kinins and prostaglandins are all implicated in the regulation of glomerular filtration rate (GRF), renal blood flow (RBF) and urinary sodium excretion. Sodium 171-177 renin Homo sapiens 4-9 6135874-6 1983 During moderate sodium restriction, plasma renin activity was low or low-normal in five of the seven patients. Sodium 16-22 renin Homo sapiens 43-48 6138931-2 1983 Stimulation or inhibition of renin at least during a normal sodium intake seems to depend mostly on the sympathetic nervous system and be mediated through beta 1-adrenoceptors. Sodium 60-66 renin Homo sapiens 29-34 6345888-3 1983 The results were compared with those of patients with primary aldosteronism and with essential hypertension where renin activity can be stimulated under similar sodium balance conditions. Sodium 161-167 renin Homo sapiens 114-119 6303176-1 1983 Recent studies suggest that sodium-dependent low-renin hypertension in animals results at least in part from sodium-potassium pump inhibition in blood vessels and heart by a humoral agent released from or influenced by the anteroventral third ventricular area of the brain. Sodium 28-34 renin Homo sapiens 49-54 6369515-1 1983 The relationship of the renin-angiotensin-aldosterone system to blood pressure and sodium homeostasis and to renal function was investigated serially in 12 patients with fulminant hepatic failure. Sodium 83-89 renin Homo sapiens 24-29 7037818-8 1982 Gross changes in sodium intake during pregnancy result in changes in active and inactive renin concentrations parallel to those observed in nonpregnant controls. Sodium 17-23 renin Homo sapiens 89-94 6315274-5 1983 If this is so, our results suggest that the renin system is an important control of both normal and high blood pressure when on a normal sodium intake. Sodium 137-143 renin Homo sapiens 44-49 6757970-2 1982 In each renin subgroup, the administration of furosemide and 2 hours upright posture induced marked increases in urinary excretion of PGE and sodium, and in plasma renin activity. Sodium 142-148 renin Homo sapiens 8-13 6281293-1 1982 Escape from the sodium-retaining action of mineralocorticoids coincides with the suppression of plasma renin and angiotensin II levels. Sodium 16-22 renin Homo sapiens 103-127 6357558-2 1983 The renin concentration of these cells is influenced by changes in sodium balance and after nephrectomy, while the renin of the fasciculata-medullary tissue is not. Sodium 67-73 renin Homo sapiens 4-9 6357565-0 1983 The renin system for long-term control over vasoconstriction and sodium-volume homeostasis in the spectrum of hypertension: three new frontiers in research. Sodium 65-71 renin Homo sapiens 4-9 6671385-6 1983 Low NA and A may participate in lowering the plasma renin activity which in PA in suppressed, sometimes disproportionately to the actual body sodium content. Sodium 142-148 renin Homo sapiens 52-57 6128546-2 1982 The other 8 patients had a high plasma renin activity which may have caused the sodium retention. Sodium 80-86 renin Homo sapiens 39-44 6751073-4 1982 On restricted sodium intake, diabetics, compared to normotensives, had reduced urinary kallikrein activity (p less than 0.01) and reduced ambulatory plasma renin activity (p less than 0.01). Sodium 14-20 renin Homo sapiens 156-161 6750618-0 1982 The role of the adrenal glands in sodium excretion evoked by centrally administered renin. Sodium 34-40 renin Homo sapiens 84-89 7037024-6 1982 It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. Sodium 27-33 renin Homo sapiens 126-131 7044119-7 1982 In the normotensive relatives of hypertensive patients, the renin system may be responsible for the decreased sodium excretory capacity. Sodium 110-116 renin Homo sapiens 60-65 7041843-0 1982 Racial difference in salivary sodium-potassium ratio in low renin essential hypertension. Sodium 30-36 renin Homo sapiens 60-65 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 46-52 renin Homo sapiens 0-5 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 108-114 renin Homo sapiens 0-5 6291819-6 1982 When the renin system is depressed, sodium loss may prevent a large drop in aldosterone levels. Sodium 36-42 renin Homo sapiens 9-14 6220764-0 1982 [Relations between the renin-angiotensin-aldosterone system and urinary elimination of sodium: study of healthy subjects in clinostatism and on a sodium-free diet]. Sodium 87-93 renin Homo sapiens 23-28 6220764-0 1982 [Relations between the renin-angiotensin-aldosterone system and urinary elimination of sodium: study of healthy subjects in clinostatism and on a sodium-free diet]. Sodium 146-152 renin Homo sapiens 23-28 7033264-7 1982 The proportion of total renin which was inactive was greater with the higher sodium intake. Sodium 77-83 renin Homo sapiens 24-29 6749346-8 1982 The mechanism of this sustained renin response several days after cessation of diuretic therapy may be best explained by a prolonged action of furosemide or by partial ongoing volume depletion with reduced sodium load to the distal nephron. Sodium 206-212 renin Homo sapiens 32-37 6754152-1 1982 A nomogram based on the relationship between plasma renin activity and urinary sodium excretion in normal subjects has been used to classify 956 patients with essential hypertension into low, medium and high renin subgroups. Sodium 79-85 renin Homo sapiens 52-57 6754154-0 1982 The salivary sodium/potassium ratio in hypertension: relation to race and plasma renin activity. Sodium 13-19 renin Homo sapiens 81-86 6764472-4 1982 Sodium loading was associated with marked suppression of plasma renin activity, aldosterone and norepinephrine, and increases in cardiac index. Sodium 0-6 renin Homo sapiens 64-69 6756698-11 1982 At the physiological level the activation and/or release of renin appears to be primarily determined by sodium-volume changes perceived by a distal tubular mechanism. Sodium 104-110 renin Homo sapiens 60-65 7047005-0 1982 Aldosterone responsiveness to angiotensin II after sodium restriction in subjects with low renin essential hypertension. Sodium 51-57 renin Homo sapiens 91-96 7047005-2 1982 The PA response to sodium restriction in relation to changes in plasma renin activity (PRA) was estimated by the ratio of PA increment to PRA increment after sodium restriction (delta PA/delta PRA). Sodium 19-25 renin Homo sapiens 71-76 7033264-8 1982 These data suggest that sodium homeostasis may influence dopaminergic modulation of renin, aldosterone, and PRL secretion and may effect the interrelationship between active and inactive renin. Sodium 24-30 renin Homo sapiens 84-89 7033264-8 1982 These data suggest that sodium homeostasis may influence dopaminergic modulation of renin, aldosterone, and PRL secretion and may effect the interrelationship between active and inactive renin. Sodium 24-30 renin Homo sapiens 187-192 7028610-6 1981 Sodium retention correlated significantly with the percent fall in urinary aldosterone only in the low-renin essential hypertension group. Sodium 0-6 renin Homo sapiens 103-108 7033970-0 1981 Effect of furosemide and dietary sodium on kidney and plasma big and small renin. Sodium 33-39 renin Homo sapiens 75-80 6757778-0 1982 Is the renin-angiotensin-aldosterone system involved in the sodium retention in the nephrotic syndrome? Sodium 60-66 renin Homo sapiens 7-12 7036720-0 1981 Sodium intake alters the effects of norepinephrine on the renin system and the kidney. Sodium 0-6 renin Homo sapiens 58-63 6800812-6 1981 It is suggested that the responsiveness of the renin-aldosterone system is abnormal during exercise in young patients with mild essential hypertension, both without and with previous intravenous sodium loading. Sodium 195-201 renin Homo sapiens 47-52 7026126-5 1981 Significant rises in plasma renin activity, plasma aldosterone concentration and renal aldosterone excretion occurred by day 2 of sodium deprivation. Sodium 130-136 renin Homo sapiens 28-33 6266727-1 1981 It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. Sodium 88-94 renin Homo sapiens 65-70 6266576-6 1981 It strongly suggested that the renin system plays an important part in maintaining blood pressure in normotensive subjects receiving normal sodium intake. Sodium 140-146 renin Homo sapiens 31-36 6789950-0 1981 Relation between arterial pressure, dietary sodium intake, and renin system in essential hypertension. Sodium 44-50 renin Homo sapiens 63-68 7020728-1 1981 The response of the renin-angiotensin system to high and low sodium diets, to standing, and to saralasin infusion was assessed before and after surgical correction of aortic coarctation in a 27-year-old man. Sodium 61-67 renin Homo sapiens 20-25 7036014-0 1981 [Effects of changes in the sodium balance on plasma catecholamines and renin activity at rest and on their response to orthostatic stimulation in arterial hypertension]. Sodium 27-33 renin Homo sapiens 71-76 7030526-0 1981 Sodium, potassium and age: possible determinants of plasma renin activity and aldosterone during childhood (age 4-16). Sodium 0-6 renin Homo sapiens 59-64 7030526-3 1981 Significant negative correlation was obtained between plasma renin activity and the 24-h urinary sodium excretion; r = -0.40, P less than 0.01. Sodium 97-103 renin Homo sapiens 61-66 7016891-7 1981 Dietary sodium restriction resulted in a further rise in plasma renin activity and a rise in urinary pH 1 aldo and 18-OH-corticosterone. Sodium 8-14 renin Homo sapiens 64-69 7024616-4 1981 The above alterations are characterized by the loss of the adequate response of the renin-angiotensin system and the adrenal cortex to the increased sodium concentration, and extracellular fluid volume in the body, as well as by the separation of the functions of these two humoral systems. Sodium 149-155 renin Homo sapiens 84-89 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 7017596-4 1981 During sodium depletion, the plasma renin activity was higher in the right renal artery (17.8 ng/ml/h) than in the left artery (9.4 ng/ml/h) and the infra-renal portion of the inferior vena cava (8.7 ng/ml/h). Sodium 7-13 renin Homo sapiens 36-41 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 6784808-2 1981 The rate constant for total leucocyte sodium efflux measured during a normal diet was significantly correlated with the plasma renin activity measured during a low sodium diet. Sodium 38-44 renin Homo sapiens 127-132 6269554-5 1981 The use of these inhibitors, especially captopril (so far the most studied), has made it clear that renin plays a part in experimental and human essential hypertension and participates in the control of arterial blood pressure in subjects with normal sodium intake. Sodium 251-257 renin Homo sapiens 100-105 6266960-4 1981 In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Sodium 23-29 renin Homo sapiens 62-67 6784808-2 1981 The rate constant for total leucocyte sodium efflux measured during a normal diet was significantly correlated with the plasma renin activity measured during a low sodium diet. Sodium 164-170 renin Homo sapiens 127-132 6784808-3 1981 Impairment of leucocyte sodium transport was significantly greater in eight patients whose plasma renin activity failed to rise into the normal range during the low sodium diet as compared with the 14 other patients, whose renin system responded normally to sodium restriction. Sodium 24-30 renin Homo sapiens 98-103 6784808-3 1981 Impairment of leucocyte sodium transport was significantly greater in eight patients whose plasma renin activity failed to rise into the normal range during the low sodium diet as compared with the 14 other patients, whose renin system responded normally to sodium restriction. Sodium 24-30 renin Homo sapiens 223-228 7037589-0 1981 Circadian rhythms of plasma renin, aldosterone and cortisol on habitual and low dietary sodium intake. Sodium 88-94 renin Homo sapiens 28-33 7013593-2 1981 Sodium restriction alone had no effect on renal clearances but did increase plasma renin activity and urinary prostaglandin E excretion. Sodium 0-6 renin Homo sapiens 83-88 7004991-10 1981 On this diet the mean creatinine clearance was 104.3 +/- 6.4 ml/min, and the mean plasma renin activity and serum aldosterone levels had decreased physiologically with the higher sodium intake. Sodium 179-185 renin Homo sapiens 89-94 7018406-5 1981 A significant inverse relationship was found between both plasma renin activity and angiotensin II, and serum sodium in the girls; a similar, although not statistically significant, relationship was seen with plasma renin activity in the boys. Sodium 110-116 renin Homo sapiens 65-70 6258416-3 1981 Plasma renin activity increased with sodium depletion (30 mEq sodium intake for 3 days after furosemide treatment) from 1.26 +/- 0.07 to 3.26 +/- 0.48 ng/ml/hr (p less than 0.001). Sodium 37-43 renin Homo sapiens 7-12 6258416-3 1981 Plasma renin activity increased with sodium depletion (30 mEq sodium intake for 3 days after furosemide treatment) from 1.26 +/- 0.07 to 3.26 +/- 0.48 ng/ml/hr (p less than 0.001). Sodium 62-68 renin Homo sapiens 7-12 6258416-6 1981 The results indicate that the renin-angiotensin system participates in the regulation of blood pressure in essential hypertension, even in the sodium-repleted state. Sodium 143-149 renin Homo sapiens 30-35 6258416-7 1981 This role of the renin-angiotensin system in blood pressure regulation becomes more crucial during sodium depletion. Sodium 99-105 renin Homo sapiens 17-22 7037337-9 1981 Basal plasma renin activity was 1.0 approximately 1.5 ng/ml/hr and increased by sodium depletion. Sodium 80-86 renin Homo sapiens 13-18 7436645-6 1980 These data suggest that sodium deprivation enhances the sympathetic nervous system activity and the orthostatic stimulation of renin release. Sodium 24-30 renin Homo sapiens 127-132 7001899-1 1980 This review considers the mechanism, prevention and therapy of sodium-dependent, low-renin, presumably volume-expanded, hypertension. Sodium 63-69 renin Homo sapiens 85-90 7009425-2 1981 Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. Sodium 158-164 renin Homo sapiens 113-118 7009425-2 1981 Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. Sodium 158-164 renin Homo sapiens 113-118 7009425-3 1981 In eight of 15 patients, significant increase of inactive renin concentration (p less than 0.01) was observed after sodium depletion. Sodium 116-122 renin Homo sapiens 58-63 7009425-5 1981 A small increase of active and inactive renin concentration was observed following sodium depletion in six essential hypertensive subjects with low plasma renin activity (PRA). Sodium 83-89 renin Homo sapiens 40-45 7009428-2 1981 Plasma renin activity (PRA) measured supine and after 4 hours of quiet ambulation, both on an ad libitum diet and on Day 4 of a 10 mEq low sodium diet, was always lower in the diabetics (31%-56% of control values). Sodium 139-145 renin Homo sapiens 7-12 6254360-3 1980 Only in the state of considerable sodium depletion does blockade of the renin system produce any untoward effect, i.e. hypotension. Sodium 34-40 renin Homo sapiens 72-77 7438475-3 1980 Hypertension with low plasma renin is consistent with sodium retention. Sodium 54-60 renin Homo sapiens 29-34 6780460-8 1980 Inactive renin was usually increased in amount in plasma of sodium-depleted normal men, but the elution volume did not change with sodium intake. Sodium 60-66 renin Homo sapiens 9-14 6780460-10 1980 Inactive renin in plasma was usually increased after sodium depletion, but the elution volume did not change. Sodium 53-59 renin Homo sapiens 9-14 7022539-5 1980 Plasma renin activity was higher in hypertensive patients despite higher exchangeable sodium levels. Sodium 86-92 renin Homo sapiens 7-12 6159648-0 1980 Specific inhibition of renin by an angiotensinogen analog: studies in sodium depletion and renin-dependent hypertension. Sodium 70-76 renin Homo sapiens 23-28 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 27-33 renin Homo sapiens 198-203 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 160-166 renin Homo sapiens 6-11 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 160-166 renin Homo sapiens 198-203 7443613-5 1980 The sodium retention was associated with suppression of plasma levels of renin and aldosterone. Sodium 4-10 renin Homo sapiens 73-78 6251761-4 1980 The development of hypotension was related to the prevailing plasma renin level, which was partly determined by the degree of sodium-depletion and the aetiology of hypertension. Sodium 126-132 renin Homo sapiens 68-73 7000394-0 1980 Renin and aldosterone in hypothyroidism: relation to excretion of sodium and potassium. Sodium 66-72 renin Homo sapiens 0-5 6998681-1 1980 The responses of renin release to three different stimuli, such as 1) head-up tilt, 2) administration of loop diuretics(bumetanide) and 3) low sodium diet + administration of bumetanide + ambulation were examined in essential hypertensive patients and normotensive subjects. Sodium 143-149 renin Homo sapiens 17-22 6992515-6 1980 After 4 months, renin was inversely correlated with serum sodium. Sodium 58-64 renin Homo sapiens 16-21 6253243-4 1980 With the renin system neutralized, blood pressure becomes exquisitely sensitive to changes in sodium balance. Sodium 94-100 renin Homo sapiens 9-14 7001263-0 1980 Influence of age and sodium intake on plasma renin activity of normal subjects. Sodium 21-27 renin Homo sapiens 45-50 7000473-0 1980 Dissociated renin-aldosterone response to acute sodium depletion in patients with a previous history of pregnancy-associated hypertension. Sodium 48-54 renin Homo sapiens 12-17 6993099-0 1980 Effect of an intravenous fluid load on urinary sodium excretion and its relation to blood pressure, blood volume and renin in hypertensive and normotensive man. Sodium 47-53 renin Homo sapiens 117-122 232024-7 1979 Prior sodium depletion abolished the specificity of the renin and depressor responses to angiotensin blockage for renovascular hypertension. Sodium 6-12 renin Homo sapiens 56-61 490250-7 1979 It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system. Sodium 61-67 renin Homo sapiens 168-173 119504-4 1979 Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Sodium 119-125 renin Homo sapiens 5-10 119504-4 1979 Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Sodium 119-125 renin Homo sapiens 43-48 510563-1 1979 The enzyme renin is the initiator of a series of steps that ultimately leads to the generation of angiotensin II, a potent pressor peptide that also has both a direct and indirect role in renal sodium conservation. Sodium 194-200 renin Homo sapiens 11-16 496101-0 1979 Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. Sodium 79-85 renin Homo sapiens 73-78 522241-0 1979 Renin response to upright posture in varying sodium balance in normal young Japanese men. Sodium 45-51 renin Homo sapiens 0-5 393503-8 1979 Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. Sodium 70-76 renin Homo sapiens 7-12 514119-4 1979 The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity. Sodium 267-273 renin Homo sapiens 323-328 395185-0 1979 Glucose-induced paradoxical hyperkalemia in patients with suppression of the renin-aldosterone system: prevention by sodium depletion. Sodium 117-123 renin Homo sapiens 77-82 395185-2 1979 Sodium restriction induced a dramatic increase in plasma renin activity (PRA) and/or plasma aldosterone (PA) in every patient, a substantial fall in the elevated serum potassium levels in 4 out of the 6 patients and a marked increase in fractional potassium excretion. Sodium 0-6 renin Homo sapiens 57-62 469152-7 1979 The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water. Sodium 146-152 renin Homo sapiens 35-40 464461-2 1979 All 32 renovascular patients on normal sodium intake had high renin-sodium profiles and renin values greater than or equal to 5 ng angiotensin I/mL.h, as compared to 20 of 64 with essential hypertension. Sodium 39-45 renin Homo sapiens 88-93 464461-2 1979 All 32 renovascular patients on normal sodium intake had high renin-sodium profiles and renin values greater than or equal to 5 ng angiotensin I/mL.h, as compared to 20 of 64 with essential hypertension. Sodium 68-74 renin Homo sapiens 62-67 396242-7 1979 These findings indicate that although renin and aldosterone secretion respond to change in sodium intake in pregnancy, the cause of the increased renin secretion of pregnancy may be secondary to the increase that occurs in prostaglandin synthesis. Sodium 91-97 renin Homo sapiens 38-43 397605-7 1979 Renin"s part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. Sodium 76-82 renin Homo sapiens 0-5 397605-8 1979 If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), renin continues to play a significant role during the chronic phase. Sodium 3-9 renin Homo sapiens 126-131 501929-8 1979 The renin-aldosterone axis in response to changes in dietary sodium and posture must be individually assessed. Sodium 61-67 renin Homo sapiens 4-9 481942-0 1979 Plasma renin activity related to sodium balance, renal function and urinary vasopressin in the newborn infant. Sodium 33-39 renin Homo sapiens 7-12 481942-4 1979 Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). Sodium 65-71 renin Homo sapiens 7-12 481942-4 1979 Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). Sodium 107-113 renin Homo sapiens 7-12 467373-1 1979 In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. Sodium 85-91 renin Homo sapiens 144-149 219051-7 1979 This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. Sodium 123-129 renin Homo sapiens 58-63 465980-4 1979 A further period of more severe sodium depletion increased plasma renin levels and the depressor effect of saralasin, but did not help to differentiate renal artery stenosis from other forms of hypertension. Sodium 32-38 renin Homo sapiens 66-71 467373-2 1979 During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. Sodium 12-18 renin Homo sapiens 156-161 110603-7 1979 These results suggest that in non-azotaemic cirrhosis with ascites the renin-angiotensin-aldosterone system is an important factor influencing sodium excretion, increased plasma renin and aldosterone concentrations are mainly due to an increased secretion rate, and total renal perfusion is not a major factor influencing renin secretion. Sodium 143-149 renin Homo sapiens 71-76 399937-3 1979 However, the BH group exhibited greater responses in terms of plasma catecholamines and plasma renin activity in response to sodium deprivation and treadmill exercise. Sodium 125-131 renin Homo sapiens 95-100 285563-0 1979 Effect of sodium loading on the renin-aldosterone system in essential hypertension. Sodium 10-16 renin Homo sapiens 32-37 214254-6 1979 Therefore, the amplitude of the elevation is predictably diminished by the rise in plasma renin consequent to prior sodium restriction, and also by preliminary receptor exposure to low dose nonpressor infusions of saralasin itself (0.01-0.1 microgram/kg per min). Sodium 116-122 renin Homo sapiens 90-95 397714-4 1979 Moderately elevated values of plasma renin activity in older salt-losers normalized after increasing the dietary sodium intake. Sodium 113-119 renin Homo sapiens 37-42 102471-8 1978 Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. Sodium 80-86 renin Homo sapiens 7-12 428287-0 1979 Renal hemodynamics and the renin--angiotensin system in cirrhosis: relationship to sodium retention. Sodium 83-89 renin Homo sapiens 27-32 156392-3 1979 Serum sodium levels decreased significantly in hypertensive patients one or two days before the peak of the hypertensive crisis and, in the Center where it was measured, plasma renin activity increased in an opposite trend to the fall of sodium. Sodium 6-12 renin Homo sapiens 177-182 384510-7 1979 The results also suggest that an increased activity of the renin-angiotensin system may be counterbalanced by sodium and fluid retention in hypertension following an acute renal allograft reaction. Sodium 110-116 renin Homo sapiens 59-64 364155-7 1978 Finally, the major functions of the renin-angiotensin system in the control of blood pressure, of sodium and water balance, and of intrarenal events, are summarized. Sodium 98-104 renin Homo sapiens 36-41 391545-2 1979 There is a parallel between water intake and plasma renin activity (PRA) in states like hypovolemia, hemorrhagia, hypotension, sodium loss, etc. Sodium 127-133 renin Homo sapiens 52-57 78048-0 1978 Big renin in plasma of healthy subjects on high sodium intake. Sodium 48-54 renin Homo sapiens 4-9 744170-10 1978 These results indicate taht pretreatment of sodium depletion is necessary to prevent the side effect caused by the agonistic pressor action of AII analogue, and also to predict renin depency in hypertensive patients efficiently. Sodium 44-50 renin Homo sapiens 177-182 400731-0 1978 Adrenal responses to pharmacological interruption of the renin-angiotensin system in sodium-restricted normal man. Sodium 85-91 renin Homo sapiens 57-62 400731-1 1978 We assessed the role of the renin-angiotensin system in the control of aldosterone secretion in response to sodium restriction in 62 normal subjects. Sodium 108-114 renin Homo sapiens 28-33 400731-2 1978 Both saralasin, an angiotensin II antagonist, and SQ 20881, a converting enzyme inhibitor, induced a dose-related decrease in plasma aldosterone levels when the renin-angiotensin system was activated by restriction of sodium intake. Sodium 218-224 renin Homo sapiens 161-166 78048-2 1978 When healthy volunteers were given first a diet containing 400 mmol sodium and then a diet containing 10 mmol sodium for 4 days the changes in salt intake stimulated large changes in active plasma-renin and smaller changes in inactive renin. Sodium 110-116 renin Homo sapiens 197-202 78048-2 1978 When healthy volunteers were given first a diet containing 400 mmol sodium and then a diet containing 10 mmol sodium for 4 days the changes in salt intake stimulated large changes in active plasma-renin and smaller changes in inactive renin. Sodium 110-116 renin Homo sapiens 235-240 666132-2 1978 In normal subjects, three components of renin release, "basal," "neural," and "sodium-sensitive," could be delineated. Sodium 79-85 renin Homo sapiens 40-45 28952-8 1978 The normal-sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low-sodium group renin and aldosterone increased more slowly but remained elevated. Sodium 11-17 renin Homo sapiens 70-75 639240-6 1978 The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg. Sodium 18-24 renin Homo sapiens 90-95 28952-9 1978 It is concluded that dietary sodium restriction increases diuretic-induced potassium loss, presumably by an increased activity of the renin-angiotensin-aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion. Sodium 29-35 renin Homo sapiens 134-139 633780-3 1978 It is suggested that renal hypotension after acute losses of sodium and extracellular fluid may also develop in patients with chronically depressed renin-angiotensin system. Sodium 61-67 renin Homo sapiens 148-153 688983-3 1978 However, when the renin-angiotensin-aldosterone system was stimulated by sodium depletion the glucose-induced paradoxical hyperkalemia was abolished and the governing role of potassium became less evident. Sodium 73-79 renin Homo sapiens 18-23 713415-2 1978 After sodium-depletion of short duration mean arterial pressure dropped more than 10 mm Hg in 9 of 25 patients with essential and in 7 of 9 patients with renin-induced hypertension. Sodium 6-12 renin Homo sapiens 154-159 713415-3 1978 After long-lasting sodium depletion the fall of mean arterial pressure exceeded 10 mm Hg in 11 of 16 patients with essential and in 8 of 9 patients with renin-induced hypertension. Sodium 19-25 renin Homo sapiens 153-158 699588-1 1978 1-Sar-8-ala-angiotensin II did not change intra-arterial pressure in 25 sodium replete hypertensive patients, whilst the pressure changes were closely related to the plasma renin level during sodium depletion (r = -0.87; n = 32). Sodium 192-198 renin Homo sapiens 173-178 148727-0 1978 The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure. Sodium 27-33 renin Homo sapiens 43-48 148727-1 1978 The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Sodium 75-81 renin Homo sapiens 91-96 148727-8 1978 This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately" increased in relationship to the sodium excess. Sodium 170-176 renin Homo sapiens 19-24 750607-1 1978 Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI), produces a prompt and profound suppression of plasma renin activity (PRA) and plasma aldosterone concentration (PA) without concomitant alterations in serum sodium and potassium concentrations. Sodium 335-341 renin Homo sapiens 231-236 754782-0 1978 [Effect of sodium depletion on plasma renin activity in blood reflux from the renal veins in essential and nephrovascular hypertension]. Sodium 11-17 renin Homo sapiens 38-43 699588-3 1978 Plasma renin is unaffected in sodium replete subjects, but increases during saralasin in sodium deplete conditions. Sodium 30-36 renin Homo sapiens 7-12 886216-0 1977 Effects of potassium chloride on plasma renin activity during sodium restriction in normal man. Sodium 62-68 renin Homo sapiens 40-45 622601-6 1978 The increase in plasma renin activity expected with sodium depletion and diuretic therapy was not blunted by propranolol. Sodium 52-58 renin Homo sapiens 23-28 563937-8 1977 To choose the most rational therapy regimen it may be useful to calculate the renin-sodium index that reflects the relationship between the plasma renin activity and the urine excretion of sodium. Sodium 84-90 renin Homo sapiens 78-83 563937-8 1977 To choose the most rational therapy regimen it may be useful to calculate the renin-sodium index that reflects the relationship between the plasma renin activity and the urine excretion of sodium. Sodium 84-90 renin Homo sapiens 147-152 902672-0 1977 Hypotensive effects of sodium volume depletion and 1-sar-8-ala-angiotensin II in relation to plasma renin in hypertensive patients. Sodium 23-29 renin Homo sapiens 100-105 902672-1 1977 The hypotensive effect of acute sodium volume depletion, produced by chlorthalidone and a low sodium diet, was inversely related to the plasma renin concentration (PRC) in 13 hypertensive patients of varying aetiology (r = 0.61; p less than 0.05); weight reduction induced by this therapy was not related to PRC (r = 0.12; p greater than 0.1). Sodium 32-38 renin Homo sapiens 143-148 902672-1 1977 The hypotensive effect of acute sodium volume depletion, produced by chlorthalidone and a low sodium diet, was inversely related to the plasma renin concentration (PRC) in 13 hypertensive patients of varying aetiology (r = 0.61; p less than 0.05); weight reduction induced by this therapy was not related to PRC (r = 0.12; p greater than 0.1). Sodium 94-100 renin Homo sapiens 143-148 902672-4 1977 The results demonstrate that acute sodium volume depletion caused similar weight loss in patients with high and low PRC values, and it would have had similar hypotensive effects but for angiotensin-induced vasoconstriction in the high renin patients. Sodium 35-41 renin Homo sapiens 235-240 640577-1 1978 The changes in plasma renin activity (PRA) and plasma aldosterone concentration (PA) in response to dietary sodium restriction and upright posture were evaluated in 7 patients with juvenile-type, insulin-dependent, uncomplicated diabetes mellitus and in 5 healthy volunteers. Sodium 108-114 renin Homo sapiens 22-27 366278-4 1978 The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." Sodium 14-20 renin Homo sapiens 110-115 366278-4 1978 The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." Sodium 77-83 renin Homo sapiens 110-115 341466-2 1978 Unstimulated plasma renin and aldosterone levels were within control range in all patients and rose significantly in response to sodium depletion. Sodium 129-135 renin Homo sapiens 20-25 742128-0 1978 [Effect of oral sodium load on the renin and aldosterone secretion in essential hypertension. Sodium 16-22 renin Homo sapiens 35-40 71600-8 1977 Thus, sodium depletion stimulates total renin release, while propranolol and clonidine produce divergent responses of active renin and prorenin, the changes in prorenin depending on the changes induced in blood-pressure. Sodium 6-12 renin Homo sapiens 40-45 599839-1 1977 We assessed the role of the renin-angiotensin system in the response of the renal circulation to restriction of sodium intake in 38 normal patients. Sodium 112-118 renin Homo sapiens 28-33 599962-0 1977 The influence of upright position and sodium restriction in the diet on plasma renin activity (PRA) and aldosteronemia in patients with chronic nephritis. Sodium 38-44 renin Homo sapiens 79-84 914228-0 1977 [Effects of acute sodium depletion on blood pressure and renin-angiotensin-aldosterone system in patients with benign essential hypertension (author"s transl)]. Sodium 18-24 renin Homo sapiens 57-62 907802-5 1977 These results demonstrate that the inhibitory effect of two different betablocking agents on renin release is not related to their cardio-selectivity and is independent of sodium balance. Sodium 172-178 renin Homo sapiens 93-98 907802-6 1977 The influence of the renin decrease on aldosterone is dependent on sodium balance and on the initial state of the renin angiotensin system. Sodium 67-73 renin Homo sapiens 21-26 874078-7 1977 Plasma renin activity showed similar increments after sodium restriction in all groups. Sodium 54-60 renin Homo sapiens 7-12 872524-13 1977 We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly. Sodium 92-98 renin Homo sapiens 43-48 14160-2 1977 The renin-angiotensin system appears to play a major role in the regulation of sodium excretion and fluid intake in a wide variety of animal species from mammals to teleosts. Sodium 79-85 renin Homo sapiens 4-9 20666-2 1977 According to the results of the plasma renin activity, we noted variations in blood volume and exchangeable sodium in order to determine the best possible treatment based on these data. Sodium 108-114 renin Homo sapiens 39-44 858175-8 1977 Renin fell during the phase of sodium gain, and remained low afterwards. Sodium 31-37 renin Homo sapiens 0-5 858175-14 1977 The long-term effects of mineralocorticoid excess on the interrelations between pressure, volume, and renin bear some resemblance to the pattern observed in patients with established essential hypertension, i.e., pressure remains elevated despite a decrease of volume, and renin is "inappropriately" suppressed in relation to the sodium and volume status. Sodium 330-336 renin Homo sapiens 102-107 191300-3 1977 This subgroup includes nearly all patients with high or "normal" renin--sodium profiles. Sodium 72-78 renin Homo sapiens 65-70 191300-7 1977 Meanwhile the validation provided by these three different pharmacologic probes portends a burgeoning clinical role for renin--sodium profiling not only in screening for renal and adrenal cortical hypertensions but also for characterizing the vasoconstrictor and volume elements involved in various individual patients and thus enabling more specific treatments of the various subtypes of essential hypertension. Sodium 127-133 renin Homo sapiens 120-125 558584-14 1977 This implies that a high sodium concentration at the macula densa stimulates renin release. Sodium 25-31 renin Homo sapiens 77-82 846064-1 1977 The role of the renin-angiotensin system in mediating the aldosterone response to sodium depletion was examined by administration of propranolol during dietary sodium restriction. Sodium 82-88 renin Homo sapiens 16-21 844248-9 1977 It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention. Sodium 191-197 renin Homo sapiens 108-113 846064-2 1977 The beta-adrenergic antagonist prevented the expected increase of plasma renin activity in response to sodium restriction in six of twelve studies. Sodium 103-109 renin Homo sapiens 73-78 846064-6 1977 It is suggested that the aldosterone response to sodium restriction is mediated not only by increased plasma renin activity and angiotensin II concentration, but also another mechanism, possibly related to increased adrenal sensitivity to angiotensin during sodium depletion. Sodium 49-55 renin Homo sapiens 109-114 857177-6 1977 It is concluded that the renin-angiotensin system in patients on chronic hemodialysis still functions as one of the adjustment mechanisms for the circulatory homeostasis, when challenged by volume loss or volume and sodium loading. Sodium 216-222 renin Homo sapiens 25-30 339673-6 1977 The results indicate that sodium retention is involved in the pathogenesis of posttransplant hypertension and suggest that an increased activity of the renin--angiotensin system is counterbalanced by an accumulation of sodium in TRAS. Sodium 219-225 renin Homo sapiens 152-157 833263-9 1977 These observations suggest that estrogen-induced increases in renin substrate do not alone account for the increases in the renin-angiotensin-aldosterone system observed during pregnancy, but rather such increases appear to represent a physiological response to increased sodium need during pregnancy. Sodium 272-278 renin Homo sapiens 62-67 837964-3 1977 The effect of ASA on urinary sodium excretion was most prominent during day time (8 a.m.-10 p.m.) and on days with low sodium intake, as confirmed by control sodium excretion and plasma renin activity. Sodium 29-35 renin Homo sapiens 186-191 341139-1 1977 Interrelationship between blood pressure, kidney function, renin-aldosterone system and body sodium content. Sodium 93-99 renin Homo sapiens 59-64 341139-5 1977 It is suggested that sodium retention may counterbalance increased activity of the renin system in KTAS. Sodium 21-27 renin Homo sapiens 83-88 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 258-264 renin Homo sapiens 180-185 613576-0 1977 [Regulation of renin secretion in saluretic-induced sodium loss]. Sodium 52-58 renin Homo sapiens 15-20 1013701-2 1976 Using this approach it was possible to show that renin via angiotensin participates actively in blood pressure maintenace, particularly following sodium depletion. Sodium 146-152 renin Homo sapiens 49-54 799552-4 1976 The renin-angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. Sodium 98-104 renin Homo sapiens 4-9 1002819-3 1976 Sodium lactate (75 mEq sodium/hr) also significantly reduced renin levels at 20-30 min (P less than 0.01). Sodium 23-29 renin Homo sapiens 61-66 1002819-4 1976 The infusion of 1/3 normal saline (25 mEq sodium/h for 2 h) produced a significant reduction (P less than 0.01) in plasma renin activity (from control levels of 5.2 +/- 0.8 to 3.1 +/- 0.6 ng/ml/h at 90 min). Sodium 42-48 renin Homo sapiens 122-127 1002819-6 1976 The observed effects of the hydrogen and calcium ions on suppressing renin release may be secondary to their known actions on renal sodium excretion. Sodium 132-138 renin Homo sapiens 69-74 1002819-7 1976 Since the infusions of calcium and hydrogen ions both result in an increased delivery of sodium to the distal segment of the nephron, the results may reflect the regulation of renin by the macula densa, a sensitive intrarenal sensor of renal tubular sodium. Sodium 89-95 renin Homo sapiens 176-181 1002819-7 1976 Since the infusions of calcium and hydrogen ions both result in an increased delivery of sodium to the distal segment of the nephron, the results may reflect the regulation of renin by the macula densa, a sensitive intrarenal sensor of renal tubular sodium. Sodium 250-256 renin Homo sapiens 176-181 980059-3 1976 Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. Sodium 93-99 renin Homo sapiens 24-29 980059-3 1976 Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. Sodium 150-156 renin Homo sapiens 24-29 980059-4 1976 However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. Sodium 66-72 renin Homo sapiens 24-29 980059-4 1976 However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. Sodium 66-72 renin Homo sapiens 123-128 980059-5 1976 In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 53-58 980059-5 1976 In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 131-136 980059-6 1976 Even the low-renin type can become renin dependent with sufficient sodium depletion. Sodium 67-73 renin Homo sapiens 13-18 980059-6 1976 Even the low-renin type can become renin dependent with sufficient sodium depletion. Sodium 67-73 renin Homo sapiens 35-40 1071607-2 1976 In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 13-18 1071607-2 1976 In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 131-136 1071607-4 1976 Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. Sodium 67-73 renin Homo sapiens 13-18 1071607-4 1976 Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. Sodium 67-73 renin Homo sapiens 35-40 10725-0 1976 Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man. Sodium 10-16 renin Homo sapiens 37-42 10725-2 1976 Sodium depletion stimulates renin release. Sodium 0-6 renin Homo sapiens 28-33 10725-3 1976 Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Sodium 78-84 renin Homo sapiens 21-26 10725-5 1976 A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. Sodium 167-173 renin Homo sapiens 123-128 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 204-210 renin Homo sapiens 180-185 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 258-264 renin Homo sapiens 286-291 185902-2 1976 A reciprocal relationship exists between sodium balance and the circulating levels of renin and angiotensin II. Sodium 41-47 renin Homo sapiens 86-91 975494-5 1976 A significant (p less than 0.05 increase in 24 h urinary aldosterone, plasma aldosterone and plasma renin activity resulted with decreased dietary sodium intake and conversely, a significant (p less than 0.05) decrease in each hormone occurred with increased dietary sodium intake. Sodium 147-153 renin Homo sapiens 100-105 1053468-6 1976 There was a general upward shift of plasma renin levels in terms of 24-hour renal sodium excretion in those who demonstrated an antihypertensive response to the drug. Sodium 82-88 renin Homo sapiens 43-48 988054-0 1976 The effects of dietary sodium on the diurnal activity of the renin-angiotensin-aldosterone system and the excretion of urinary electrolytes. Sodium 23-29 renin Homo sapiens 61-66 990387-0 1976 Effect of acute sodium or potassium depletion on plasma renin activity in haemodialysed patients. Sodium 16-22 renin Homo sapiens 56-61 181394-2 1976 High exchangeable sodium (56.7 meq/kg vs. 45-55 meq/kg in controls) was associated with a low plasma renin activity (6 ng/1/min vs. 26 +/- 3.1 in controls) and reduced aldosterone secretion rate (5.56 mug/day; normal: 50-150 mug per day)). Sodium 18-24 renin Homo sapiens 101-106 999213-6 1976 Plasma renin activity values correlated positively with 12-hour urinary VMA excretion (p less than 0.01) and negatively with 6-hour urinary sodium excretion (p less than 0.05) before and after Sauna, suggesting the role of catecholamines and sodium depletion in renin response in Sauna. Sodium 140-146 renin Homo sapiens 7-12 999213-6 1976 Plasma renin activity values correlated positively with 12-hour urinary VMA excretion (p less than 0.01) and negatively with 6-hour urinary sodium excretion (p less than 0.05) before and after Sauna, suggesting the role of catecholamines and sodium depletion in renin response in Sauna. Sodium 242-248 renin Homo sapiens 7-12 937361-3 1976 Studies of his renal function suggest that the basic pathophysiologic defect was an abnormality in proximal tubular sodium reabsorption which led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone axis. Sodium 116-122 renin Homo sapiens 220-225 940019-0 1976 Plasma renin activity in normal children: its relationship to age and rates of excretion of sodium and potassium. Sodium 92-98 renin Homo sapiens 7-12 939234-2 1976 A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. Sodium 150-156 renin Homo sapiens 79-84 976606-1 1976 Plasma renin activity (PRA) was determined in 48 patients with diabetes mellitus in sodium balance on a 10-20 mEq. Sodium 84-90 renin Homo sapiens 7-12 943925-5 1976 Hypertensive children with low and high plasma renin activity were found to have an inappropriately high level of urinary aldosterone excretion in relation to urinary sodium excretion. Sodium 167-173 renin Homo sapiens 47-52 178461-2 1976 Patients with essential hypertension had been previously studied and known to have normal responses of plasma renin activity to sodium restriction and upright posture. Sodium 128-134 renin Homo sapiens 110-115 1020762-5 1976 Sodium depletion abolished pressor responses and resulted in depressor responses in 64 per cent of the patients with normal renin values. Sodium 0-6 renin Homo sapiens 124-129 1261208-2 1976 Suppression of the renin-aldosterone system by expansion of the extracellular fluid volume with extra sodium and mineralocorticoid for 6 days was studied in nine young men with very mild essential hypertension and in ten normotensive young men. Sodium 102-108 renin Homo sapiens 19-24 180059-7 1976 Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. Sodium 100-106 renin Homo sapiens 29-34 180059-8 1976 However, the mean high sodium level in the normal renin essential hypertension group (11.6+/-1.6 ng/dl) was significantly greater (P is less than 0.001) than in the control group (5.4+/-0.7 ng/dl). Sodium 23-29 renin Homo sapiens 50-55 940907-2 1976 This study suggests that emotional stimuli, which produce cardioacceleration, may also cause increased renin secretion, thus providing a mechanism by which factors operating through the mind and sodium intake could summate in the production of hypertension. Sodium 195-201 renin Homo sapiens 103-108 932525-7 1976 Response of renin activity to sodium restriction and standing was 73 per cent of that of the younger age group. Sodium 30-36 renin Homo sapiens 12-17 57453-12 1976 It is concluded that sodium depletion induced "renin dependency" of B.P. Sodium 21-27 renin Homo sapiens 47-52 987139-0 1976 [The mechanism of paradoxical response of plasma renin activity to sodium in patients with edema]. Sodium 67-73 renin Homo sapiens 49-54 1249473-10 1976 Plasma renin activity and urinary aldosterone excretion rose progressively with the two levels of sodium restriction. Sodium 98-104 renin Homo sapiens 7-12 174834-8 1976 Both plasma aldosterone concentration and plasma renin activity rose on tilting in both sodium replete and sodium depleted subjects. Sodium 88-94 renin Homo sapiens 49-54 940271-1 1976 Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). Sodium 70-76 renin Homo sapiens 38-43 940271-1 1976 Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). Sodium 252-258 renin Homo sapiens 38-43 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 41-47 renin Homo sapiens 12-17 1244226-1 1976 An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women. Sodium 50-56 renin Homo sapiens 73-78 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 45-50 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 71-76 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 71-76 10715-1 1976 The relationship between blood pressure, plasma renin, plasma renin substrate and exchangeable sodium in chronic hemodialysis patients. Sodium 95-101 renin Homo sapiens 62-67 10715-8 1976 These results strongly suggest that the renin-angiotensin system is the most important factor involved in the pathogenesis of hypertension in end-stage renal disease, when sodium balance is adequately controlled. Sodium 172-178 renin Homo sapiens 40-45 188010-7 1976 Despite the increased level of activity of the renin-angiotensin system in normal pregnancy, sodium homeostasis is maintained. Sodium 93-99 renin Homo sapiens 47-52 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 41-47 renin Homo sapiens 201-206 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 36-42 renin Homo sapiens 143-148 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 82-88 renin Homo sapiens 12-17 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 36-42 renin Homo sapiens 294-299 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 68-74 renin Homo sapiens 143-148 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 82-88 renin Homo sapiens 201-206 1019166-3 1976 They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension. Sodium 100-106 renin Homo sapiens 42-47 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 108-114 renin Homo sapiens 8-13 1019167-3 1976 In 12 tests performed after sodium depletion, the decrease in mean arterial pressure ranged from 13 to 76 mm Hg and showed a significant correlation with the plasma renin concentration prevailing immediately before the infusion of the drug (r = 0.81; p less than 0.001). Sodium 28-34 renin Homo sapiens 165-170 1192047-6 1975 The findings emphasise the need to relate data from patients to age-matched control values before attempting interpretation and suggest that sodium depletion is a more potent stimulator of renin-aldosterone release than renovascular disease or renal scarring in children. Sodium 141-147 renin Homo sapiens 189-194 1215976-1 1975 Plasma renin activity was found to correlate inversely with exchangeable sodium or blood volume in both normotensive and hypertensive hemodialysis patients. Sodium 73-79 renin Homo sapiens 7-12 1208596-0 1975 The relationship between sodium excretion and renin secretion by the perfused kidney. Sodium 25-31 renin Homo sapiens 46-51 1208596-6 1975 These results provide new evidence for the hypothesis that the rate at which sodium is delivered to the macula densa is an important determinant of the rate of renin secretion. Sodium 77-83 renin Homo sapiens 160-165 1239966-4 1975 The increase of renin and plasma aldosterone was correlated inversely to urinary sodium-potassium-ratio. Sodium 81-87 renin Homo sapiens 16-21 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 130-136 renin Homo sapiens 8-13 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 130-136 renin Homo sapiens 8-13 168714-9 1975 Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Sodium 109-115 renin Homo sapiens 73-78 1190091-2 1975 Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Sodium 79-85 renin Homo sapiens 7-12 1166859-9 1975 In contrast, suppression of the renin level to normal was demonstrated by sodium loading. Sodium 74-80 renin Homo sapiens 32-37 1192694-2 1975 Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. Sodium 124-130 renin Homo sapiens 74-79 168714-10 1975 Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. Sodium 94-100 renin Homo sapiens 152-157 168714-11 1975 When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake. Sodium 103-109 renin Homo sapiens 59-64 1162906-0 1975 [Relationship of plasma renin activity and exchangeable sodium in various types of hypertension]. Sodium 56-62 renin Homo sapiens 24-29 1098253-7 1975 Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. Sodium 171-177 renin Homo sapiens 101-106 1132118-5 1975 Simultaneous plasma renin activities were elevated and comparable to those of civilized subjects placed for brief periods on 10 mEq sodium diets. Sodium 132-138 renin Homo sapiens 20-25 802649-12 1975 This study suggests that the decrease in plasma renin activity was related to the lowering of the heart rate rather than to sodium retention and that adrenergic-blocking agents can impair the normal relationship between stroke index and plasma volume, between plasma volume and plasma renin activity, and between plasma renin activity and plasma aldosterone. Sodium 124-130 renin Homo sapiens 48-53 1147438-1 1975 Effects of potassium and sodium replacement on the renin-angiotensin-aldosterone system. Sodium 25-31 renin Homo sapiens 51-56 166090-6 1975 These findings suggest that beta-adrenergic receptors have a role in mediating the effects of sodium depletion upon renin secretion and adenyl cyclase activity. Sodium 94-100 renin Homo sapiens 116-121 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 106-112 renin Homo sapiens 193-198 172005-7 1975 These results confirm that acute sodium depletion stimulates aldosterone secretion by the way of renin angiotensin system then ACTH acts directly on the adrenal cortex. Sodium 33-39 renin Homo sapiens 97-102 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 281-287 renin Homo sapiens 193-198 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 281-287 renin Homo sapiens 193-198 235559-20 1975 These studies indicate that there is a close correlation of bradykinin levels with renin activity and angiotensin II, in both acute sodium loading and assumption of upright posture, suggesting that these two systems may be physiologically interrelated. Sodium 132-138 renin Homo sapiens 83-88 1135521-0 1975 Marked elevation of plasma renin activity during post diuretic sodium conservation in furosemide stimulated subjects. Sodium 63-69 renin Homo sapiens 27-32 234666-10 1975 The cardiac attacks in these five patients all occurred during or shortly after procedures, such as sodium-depleting dialysis, renal artery surgery, or diazoxide administration, known to cause increase in plasma concentrations of renin and angiotensin II. Sodium 100-106 renin Homo sapiens 230-235 1152349-7 1975 Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. Sodium 111-117 renin Homo sapiens 74-79 1232875-3 1975 Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). Sodium 107-113 renin Homo sapiens 50-55 172003-3 1975 The sodium depletion induced by furosemide during continuous ACTH infusion increases plasma renin activity but does not change PA. Sodium 4-10 renin Homo sapiens 92-97 1116335-3 1975 First, renin activity was measured in hospital patients after 5 days of sodium restriction and 3 h ambulation. Sodium 72-78 renin Homo sapiens 7-12 234677-8 1975 Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. Sodium 168-174 renin Homo sapiens 101-106 4428983-0 1974 [Effect of calcium and sodium in the production of renin in vitro: action of cycloheximide]. Sodium 23-29 renin Homo sapiens 51-56 165438-3 1975 Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. Sodium 134-140 renin Homo sapiens 70-75 4360859-0 1974 A specific role for saline or the sodium ion in the regulation of renin and aldosterone secretion. Sodium 34-40 renin Homo sapiens 66-71 4360859-2 1974 The present study was performed to determine whether sodium has an action apart from volume in the regulation of the secretion of renin and aldosterone. Sodium 53-59 renin Homo sapiens 130-135 4360859-13 1974 The data support a specific role for volume expansion with saline or the sodium ion per se in the regulation of renin and aldosterone. Sodium 73-79 renin Homo sapiens 112-117 4355704-1 1973 An abnormal relation between sodium and the renin-angiotensin system. Sodium 29-35 renin Homo sapiens 44-49 4375892-0 1974 The relationship between the plasma concentrations of renin and angiotensin with total exchangeable sodium in hypertension. Sodium 100-106 renin Homo sapiens 54-59 4752309-3 1973 Plasma renin concentration was inversely related to exchangeable sodium in the responsive group but was inappropriately high for the level of exchangeable sodium in the resistant group. Sodium 65-71 renin Homo sapiens 7-12 4752309-3 1973 Plasma renin concentration was inversely related to exchangeable sodium in the responsive group but was inappropriately high for the level of exchangeable sodium in the resistant group. Sodium 155-161 renin Homo sapiens 7-12 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 85-90 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 85-90 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4120488-0 1973 Abnormal relation between exchangeable sodium and the renin-angiotensin system in malignant hypertension and in hypertension with chronic renal failure. Sodium 39-45 renin Homo sapiens 54-59 4522176-0 1973 Renin suppression in hypertension in relation to body fluid volumes, patterns of sodium excretion and renal haemodynamics. Sodium 81-87 renin Homo sapiens 0-5 4700008-1 1973 Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Sodium 84-90 renin Homo sapiens 7-12 4700008-1 1973 Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Sodium 103-109 renin Homo sapiens 7-12 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 91-97 renin Homo sapiens 65-70 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 158-164 renin Homo sapiens 131-136 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 158-164 renin Homo sapiens 131-136 4338644-0 1972 [Regulation of the renin-angiotensin system in congestive heart failure: indications for a total body sodium-dependent regulation of the renin secretion]. Sodium 102-108 renin Homo sapiens 19-24 5056660-12 1972 From these studies, it is concluded that plasma renin activity is the dominant factor controlling plasma aldosterone when sodium-depleted normal subjects are acutely repleted. Sodium 122-128 renin Homo sapiens 48-53 4343575-0 1972 Renin, angiotensin II, and adrenal corticosteroid relationships during sodium deprivation and angiotensin infusion in normotensive and hypertensive man. Sodium 71-77 renin Homo sapiens 0-5 5032511-0 1972 Effects of change in posture and of sodium depletion on plasma levels of vasopressin and renin in normal human subjects. Sodium 36-42 renin Homo sapiens 89-94 4338644-0 1972 [Regulation of the renin-angiotensin system in congestive heart failure: indications for a total body sodium-dependent regulation of the renin secretion]. Sodium 102-108 renin Homo sapiens 137-142 5008533-0 1972 The effects of sodium loading and deprivation on plasma renin and plasma and urinary aldosterone in hypertension. Sodium 15-21 renin Homo sapiens 56-61 5009112-7 1972 Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. Sodium 131-137 renin Homo sapiens 79-84 5107275-0 1971 [Influence of sodium concentration on the release of renin from kidney cortex slices and isolated glomeruli]. Sodium 14-20 renin Homo sapiens 53-58 5560670-0 1971 The effect of sodium and calcium on renin release in vitro. Sodium 14-20 renin Homo sapiens 36-41 4340714-0 1972 [Activation of renin in the juxtaglomerular apparatus by tubular sodium in the macula densa segment]. Sodium 65-71 renin Homo sapiens 15-20 4328882-5 1971 Furthermore, changes in aldosterone secretory rate and levels of circulating renin produced by varying dietary sodium intake, did not alter sodium influx or fractional sodium outflux in either patients with Liddle"s syndrome or normal subjects. Sodium 111-117 renin Homo sapiens 77-82 5087817-0 1971 Effects of hemorrhage and chronic sodium depletion on hepatic clearance of renin. Sodium 34-40 renin Homo sapiens 75-80 5142557-0 1971 Effect of sodium and osmotic concentration on renin release by renal cortical slices in vitro. Sodium 10-16 renin Homo sapiens 46-51 4319970-8 1970 However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance. Sodium 163-169 renin Homo sapiens 97-102 5156048-0 1971 [Relation between sodium excretion and renin plasma level on physiologic and pathologic conditions]. Sodium 18-24 renin Homo sapiens 39-44 5539024-0 1971 The relative effects of serum sodium concentration and the state of body fluid balance on renin secretion. Sodium 30-36 renin Homo sapiens 90-95 4319970-12 1970 The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport. Sodium 116-122 renin Homo sapiens 33-38 4317384-4 1970 On a 10 mEq sodium intake, the increase in excretion and secretion rates of aldosterone in the hypertensive patients could be correlated with plasma renin activity (PRA). Sodium 12-18 renin Homo sapiens 149-154 5523457-0 1970 [The possibility of stimulation and suppression of renin secretion by sodium deprivation and sodium loading in primary and renal hypertension]. Sodium 70-76 renin Homo sapiens 51-56 5699946-0 1968 Plasma renin activity in relation to serum sodium concentration and body fluid balance. Sodium 43-49 renin Homo sapiens 7-12 5751263-2 1968 Effect of the plasma sodium reduction on renin secretion]. Sodium 21-27 renin Homo sapiens 41-46 5819296-0 1969 Effect of sodium depletion on renin activity of renal venous plasma in renovascular hypertension. Sodium 10-16 renin Homo sapiens 30-35 5648055-0 1968 Renin release: relation to renal sodium load and dissociation from hemodynamic changes. Sodium 33-39 renin Homo sapiens 0-5 5730691-0 1968 [Regulation of renin secretion in sodium deficiency]. Sodium 34-40 renin Homo sapiens 15-20 5926083-0 1966 Changes in plasma aldosterone, cortisol, corticosterone, and renin concentration in a patient with sodium-losing renal disease. Sodium 99-105 renin Homo sapiens 61-66 5642688-0 1968 Plasma renin activity and aldosterone secretion in hypertensive patients during high and low sodium intake and administration of diuretic. Sodium 93-99 renin Homo sapiens 7-12 5651121-0 1968 Effect of nephrectomy and a low sodium diet on the increase in plasma renin levels produced by hemorrhage. Sodium 32-38 renin Homo sapiens 70-75 4890788-0 1968 [Regulation of renin secretion in sodium deficiency]. Sodium 34-40 renin Homo sapiens 15-20 6023776-5 1967 Concomitant measurements of endogenous creatinine clearance and the rates of excretion of sodium and potassium suggest that a fall in renal arterial perfusion resulting from upright posture induces increased release of renin and the subsequent secondary stimulation of aldosterone secretion. Sodium 90-96 renin Homo sapiens 219-224 5639033-0 1968 Plasma renin in chronic experimental heart failure and during renal sodium "escape" from mineralocorticoids. Sodium 68-74 renin Homo sapiens 7-12 4296172-0 1968 Hirano J, Masson GM: Effects of dietary sodium on hypertensive disease caused by renin. Sodium 40-46 renin Homo sapiens 81-86 6021207-4 1967 In normal subjects the stimuli of upright posture and of sodium depletion both resulted in increases in urinary catecholamines, plasma renin activity, and urinary aldosterone. Sodium 57-63 renin Homo sapiens 135-140 5937540-0 1966 Relation of plasma renin to sodium balance and arterial pressure in experimental renal hypertension. Sodium 28-34 renin Homo sapiens 19-24 33328060-4 2020 Vasodilation also results in activation of the renin-angiotensin-aldosterone axis, which combined with changing tubular handling causes alterations in total body stores of electrolytes and total body water, resulting in a lower serum sodium concentration. Sodium 234-240 renin Homo sapiens 47-52 33085785-1 2021 AIM: Plasma renin activity (PRA) is regarded as a marker of sodium and fluid homeostasis in patients with primary hypertension. Sodium 60-66 renin Homo sapiens 12-17 33824491-1 2021 The intrarenal renin-angiotensin system is critical for the regulation of tubule sodium reabsorption, renal haemodynamics and blood pressure. Sodium 81-87 renin Homo sapiens 15-20 33824491-7 2021 Furthermore, binding of prorenin and renin to the prorenin receptor in the collecting duct evokes a number of responses, including the non-proteolytic enzymatic activation of prorenin to produce ANGI from proximal tubule-derived angiotensinogen, which is then converted into ANGII by luminal angiotensin-converting enzyme; stimulation of the epithelial sodium channel (ENaC) in principal cells; and activation of intracellular pathways linked to the upregulation of cyclooxygenase 2 and profibrotic genes. Sodium 353-359 renin Homo sapiens 27-32 33824491-8 2021 These findings suggest that dysregulation of the renin-angiotensin system in the collecting duct contributes to the development of hypertension by enhancing sodium reabsorption and the progression of kidney injury. Sodium 157-163 renin Homo sapiens 49-54 33605160-13 2021 Further clinical investigation of novel and approved medications that target low renin physiology such as epithelial sodium channel inhibitors and mineralocorticoid receptor antagonists may be paramount in improving hypertension control in AAs. Sodium 117-123 renin Homo sapiens 81-86 33842863-0 2021 Influence of sodium intake and change in sodium intake on plasma-renin in man. Sodium 13-19 renin Homo sapiens 65-70 33842863-0 2021 Influence of sodium intake and change in sodium intake on plasma-renin in man. Sodium 41-47 renin Homo sapiens 65-70 33842863-1 2021 Background: Low sodium intake stimulates the production and activity of renin. Sodium 16-22 renin Homo sapiens 72-77 33842863-2 2021 The aim is to analyse the association between a large range of sodium intake and the plasma renin activity (PRA). Sodium 63-69 renin Homo sapiens 92-97 33216460-9 2021 Patients in the lower renin tertile had higher blood pressure and plasma sodium concentration (all P < 0.05). Sodium 73-79 renin Homo sapiens 22-27 14015990-0 1963 Influence of sodium loading and sodium depletion on plasma-renin in man. Sodium 13-19 renin Homo sapiens 59-64 14015990-0 1963 Influence of sodium loading and sodium depletion on plasma-renin in man. Sodium 32-38 renin Homo sapiens 59-64 33735863-14 2021 In addition, each increase in urinary sodium excretion by 2 SDs at year 1 increased prorenin and renin levels by 4 and 5% per year, respectively. Sodium 38-44 renin Homo sapiens 87-92 33350197-11 2020 We obtained 21 key targets, 154 signal pathways, and 382 biological processes in topological, GO, and KEGG enrichment analysis of the protein interaction network, and in the comprehensive analysis, it was found that Zuomua Decoction could reduce blood pressure by regulating renin angiotension aldosterone system, balancing the concentration of intracellular calcium and sodium ions and regulating vasoconstriction and relaxation. Sodium 371-377 renin Homo sapiens 275-280 31503134-9 2020 Plasma renin activity correlated negatively with sweat sodium (rs = -0.43, P = 0.012) and muscle sodium levels (rs = -0.42, P < 0.001). Sodium 55-61 renin Homo sapiens 7-12 31503134-9 2020 Plasma renin activity correlated negatively with sweat sodium (rs = -0.43, P = 0.012) and muscle sodium levels (rs = -0.42, P < 0.001). Sodium 97-103 renin Homo sapiens 7-12 31344212-1 2019 The renin-angiotensin-aldosterone system modulates volume, sodium and potassium homeostasis. Sodium 59-65 renin Homo sapiens 4-9 30407370-3 2019 Our objective was to evaluate the impact of renin angiotensin system activation, on hemodynamic deficiency and renal outcome in patient with septic shock and to assess whether urinary sodium could be a reliable test for high plasma renin concentration screening. Sodium 184-190 renin Homo sapiens 232-237 31261774-1 2019 Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin-angiotensin-aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). Sodium 193-199 renin Homo sapiens 144-149 31344212-2 2019 In the setting of a high sodium diet, up to 30% of patients with hypertension have a low or suppressed renin and increased volume. Sodium 25-31 renin Homo sapiens 103-108 30661474-12 2019 These data suggest that reducing sodium from 2300 to 1000 mg/d stimulates the renin-angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults. Sodium 33-39 renin Homo sapiens 78-83 30354328-8 2018 Standard renin-angiotensin-aldosterone system phenotyping confirmed the expected response to sodium loading. Sodium 93-99 renin Homo sapiens 9-14 30661474-3 2019 Extremely low-sodium diets (<=500 mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow. Sodium 14-20 renin Homo sapiens 68-73 30661474-10 2019 Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P<0.01 for all) but did not alter mean arterial pressure (78+-2 versus 77+-2 mm Hg, P=0.56), muscle sympathetic nerve activity (13.9+-1.3 versus 13.9+-0.8 bursts/min, P=0.98), or plasma/urine norepinephrine. Sodium 9-15 renin Homo sapiens 39-44 29902069-7 2019 The associations between the plasma renin activity and blood-pressure outcomes were evident in adults with especially high urine sodium excretion. Sodium 129-135 renin Homo sapiens 36-41 29902069-8 2019 CONCLUSION: Low plasma renin activity was associated with the development of hypertension in the middle-aged Asian population, especially in peoples with high sodium intake. Sodium 159-165 renin Homo sapiens 23-28 29758100-4 2018 Most often, low-renin levels are expression of a physiological response to sodium-volume overload, but also a significant number of secondary hereditary or acquired conditions falls within this category. Sodium 75-81 renin Homo sapiens 16-21 28814103-7 2018 A significant negative linear correlation was demonstrated between serum sodium and plasma renin activity ( P = 0.005) and direct renin concentration ( P = 0.015) and between estimated glomerular filtration rate and aldosterone measured using radioimmunoassay ( P = 0.02) and immunochemiluminometric assay ( P = 0.016). Sodium 73-79 renin Homo sapiens 91-96 30145856-2 2018 The main factor of ascites formation is renal sodium retention due to activation of the renin-angiotensin-aldosterone system and sympathetic nervous system by the reduced effective volume secondary to splanchnic arterial vasodilation. Sodium 46-52 renin Homo sapiens 88-93 30029710-5 2018 Most of articles in this review reported that 2.6-3 g/day of dietary sodium is effective for decreased BNP, renin, and aldosterone (neurohormonal) plasma levels in patients with HF. Sodium 69-75 renin Homo sapiens 108-113 29727629-2 2018 BACKGROUND: The renin angiotensin system (RAS) and the renal dopaminergic system (RDS) act as autocrine and paracrine systems to regulate renal sodium management and inflammation and their alterations have been associated to hypertension and renal damage. Sodium 144-150 renin Homo sapiens 16-21 28814103-8 2018 A significant negative linear correlation existed between urine sodium and plasma renin activity ( P = 0.04) and aldosterone measured using radioimmunoassay ( P = 0.045). Sodium 64-70 renin Homo sapiens 82-87 28930524-2 2018 Hyperinsulinemia may increase cardiovascular (CV) risk through its promotion of hypertension, which is possibly a result of chronic enhancement of sympathetic nervous system activity, stimulation of the renin-angiotensin-aldosterone system leading to increased renal tubular sodium reabsorption, modulating cation transport, or inducing vascular smooth muscle cell hypertrophy. Sodium 275-281 renin Homo sapiens 203-208 29433578-2 2018 Identifying the contribution of intravascular volume and serum renin in maintaining BP levels could help tailor more effective hypertension treatment, whether acting on the control of intravascular volume or sodium balance, or acting on the effects of the renin-angiotensin-aldosterone system (RAAS) on the kidney. Sodium 208-214 renin Homo sapiens 63-68 29433578-11 2018 Thus, identifying the contribution of intravascular volume and serum renin in maintaining BP levels could help tailor more effective hypertension treatment, whether by acting on the control of intravascular volume or sodium balance, or by acting on the effects of the RAAS on the kidney. Sodium 217-223 renin Homo sapiens 69-74 29305116-3 2018 Plasmin activates the epithelial sodium channel in the collecting ducts potentially causing impaired sodium excretion, suppression of the renin-angiotensin-aldosterone system, and hypertension in PE. Sodium 33-39 renin Homo sapiens 138-143 29360682-13 2018 CONCLUSION: Considering that the renin-angiotensin pathway plays a central role in blood pressure and plasma sodium concentration, and our observation that ACE and PTPRD expression increased over the spectrum of childhood development, this finding could potentially impact the dosing of an entire class of drugs known as ACE-inhibitors in pediatric patients. Sodium 109-115 renin Homo sapiens 33-38 28417649-1 2017 Sodium retention in cirrhosis is associated with changes in the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the glomerular filtration rate (GFR). Sodium 0-6 renin Homo sapiens 64-69 28905546-4 2017 The low renin hypertension phenotype seems to be caused by an increase in sodium retention at renal level. Sodium 74-80 renin Homo sapiens 8-13 28772209-1 2017 Renin-angiotensin-aldosterone system (RAAS) is a vital system of human body, as it maintains plasma sodium concentration, arterial blood pressure and extracellular volume. Sodium 100-106 renin Homo sapiens 0-5 28778258-2 2017 Regardless of its source, high sodium intake can both lead to hypertension and reduce the efficacy of renin-angiotensin-aldosterone system inhibitors, which are currently guideline-recommended treatments for hypertension, chronic kidney disease, and heart failure. Sodium 31-37 renin Homo sapiens 102-107 28566337-7 2017 When participants in the clinical study were maintained on a high sodium balance, renin activity progressively declined with older age, whereas serum and urinary aldosterone did not significantly decline. Sodium 66-72 renin Homo sapiens 82-87 27424689-8 2016 The renin-angiotensin-aldosterone system of VLBW infants seems to be able, even immediately after birth, to respond to variations of plasma sodium concentrations; measurement of UAE constitutes an interesting method to determine aldosterone production in VLBW infants. Sodium 140-146 renin Homo sapiens 4-9 28501983-4 2017 Evolutionarily, sodium retention mechanisms in the context of low dietary sodium provided a survival advantage and are highly conserved, exemplified by the renin-angiotensin system. Sodium 16-22 renin Homo sapiens 156-161 28501983-7 2017 From these perspectives, several mechanisms can be envisioned whereby a low-sodium diet could potentially cause harm, including the renin-angiotensin system and the sympathetic nervous system. Sodium 76-82 renin Homo sapiens 132-137 28302554-1 2017 BACKGROUND: The renin-angiotensin system (RAS) plays an important role in regulating blood pressure and controlling sodium levels in the blood. Sodium 116-122 renin Homo sapiens 16-21 28130379-6 2017 Changes in sodium levels in patients with ultrafiltration were negatively correlated to those in serum creatinine and plasma renin activity. Sodium 11-17 renin Homo sapiens 125-130 27841780-2 2017 Blacks have a greater propensity to salt sensitivity and suppressed plasma renin suggesting a predisposition to sodium retention. Sodium 112-118 renin Homo sapiens 75-80 27428770-12 2016 Milder phenotypes of PA, where PRA is not as suppressed, are most susceptible to dietary sodium influences on renin and ARR. Sodium 89-95 renin Homo sapiens 110-115 27822054-12 2016 Local inhibition of the renin-angiotensin-aldosterone system secondary to increased delivery of sodium to the juxtaglomerular apparatus during SGLT2 inhibition has also been postulated. Sodium 96-102 renin Homo sapiens 24-29 27111173-8 2016 In the meta-analysis, the standard mean difference (SMD) of renin level by sodium intake reduction was 1.26 (95% CI: 1.08 to 1.44, Z=12.80, P<0.001, I(2)=87%). Sodium 75-81 renin Homo sapiens 60-65 27981497-14 2017 In addition, canagliflozin decreased plasma ANP and NT-proBNP levels and increased plasma renin activity, which may be a compensatory mechanism for sodium retention, leading to subsequent urine output recovery. Sodium 148-154 renin Homo sapiens 90-95 27836073-2 2016 It was hypothesized that primary renal sodium retention blunted the reactivity of the renin-angiotensin-aldosterone system to changes in salt intake in preeclampsia (PE). Sodium 39-45 renin Homo sapiens 86-91 27111173-0 2016 Effect of sodium intake on renin level: Analysis of general population and meta-analysis of randomized controlled trials. Sodium 10-16 renin Homo sapiens 27-32 27111173-1 2016 BACKGROUND: We evaluated the association between sodium intake and plasma renin levels in the cross sectional study and meta-analysis of randomized controlled trials, whether there is a persistent elevation of plasma renin by longer-term sodium intake restriction. Sodium 49-55 renin Homo sapiens 74-79 25744274-2 2016 Both vitamin D receptor activator (VDRA) treatment and dietary sodium restriction potentiate the efficacy of renin-angiotensin-aldosterone-system (RAAS) blockade to reduce albuminuria. Sodium 63-69 renin Homo sapiens 109-114 26803690-0 2016 Effects of Dietary Sodium Restriction in Kidney Transplant Recipients Treated With Renin-Angiotensin-Aldosterone System Blockade: A Randomized Clinical Trial. Sodium 19-25 renin Homo sapiens 83-88 26803690-1 2016 BACKGROUND: In patients with chronic kidney disease receiving renin-angiotensin-aldosterone system (RAAS) blockade, dietary sodium restriction is an often-used treatment strategy to reduce blood pressure (BP) and albuminuria. Sodium 124-130 renin Homo sapiens 62-67 25805925-3 2015 Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone (ADH). Sodium 87-93 renin Homo sapiens 146-151 27143858-1 2016 A low sodium diet enhances the hemodynamic effect of renin-angiotensin system blockers. Sodium 6-12 renin Homo sapiens 53-58 25977313-1 2016 The renin-angiotensin-aldosterone (RAAS) and renal dopaminergic systems interact to maintain sodium balance. Sodium 93-99 renin Homo sapiens 4-9 26450935-2 2015 Both vitamin D and sodium intake interact with the renin-angiotensin-aldosterone system. Sodium 19-25 renin Homo sapiens 51-56 26240299-9 2015 The effect of sodium restriction was higher in the cohorts including patients on concomitant renin-angiotensin-aldosterone system-blocking therapy, in the studies with intervention lasting at least 2 weeks, and among participants with evidence of kidney damage. Sodium 14-20 renin Homo sapiens 93-98 26240299-12 2015 CONCLUSIONS: This meta-analysis indicates that sodium intake reduction markedly reduces albumin excretion, more so during concomitant renin-angiotensin-aldosterone system-blocking therapy and among patients with kidney damage. Sodium 47-53 renin Homo sapiens 134-139 26524901-8 2015 An increased sodium concentration inside the brain activates epithelial sodium channels and the renin-angiotensin-aldosterone system in the brain. Sodium 13-19 renin Homo sapiens 96-101 26871780-0 2016 Low Response of Renin-Angiotensin System to Sodium Intake Intervention in Chinese Hypertensive Patients. Sodium 44-50 renin Homo sapiens 16-21 26871780-2 2016 However, the influence of short-term sodium intake intervention in the response of renin-angiotensin system (RAS) on hypertensive patients is still unclear. Sodium 37-43 renin Homo sapiens 83-88 27431273-0 2016 A high sodium intake reduces antiproteinuric response to renin-angiotensin-aldosterone system blockade in kidney transplant recipients. Sodium 7-13 renin Homo sapiens 57-62 26552350-3 2015 MATERIALS AND METHODS: We created conditional deletion of CREB in mice with low-sodium diet, specifically in renin cells of the kidney. Sodium 80-86 renin Homo sapiens 109-114 26552350-6 2015 RESULTS: With low-sodium diet, renin was expressed along the whole wall of the afferent glomerular arterioles in wild-type mice, while there was no increase or even decrease in renin expression in CREB-specific deletion mice; RNA level of renin in cultured cells decreased by 50% with single knock-down of CREB, CBP, or p300, and decreased 70% with triple knock-down of CREB, CBP, and p300. Sodium 18-24 renin Homo sapiens 31-36 26471758-14 2015 Our data also suggest that the relationship between renal handling of sodium and urinary renin is sexually dimorphic. Sodium 70-76 renin Homo sapiens 89-94 26090330-3 2015 Increasing intake of salt leads to abnormal transport of sodium ions at the cellular level with activation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Sodium 57-63 renin Homo sapiens 145-150 25908470-6 2015 The additional autocrine and paracrine activities of adipose tissue contribute to inappropriate activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system that promote kidney microvascular remodeling, stiffness, and sodium (Na(+)) retention that in turn promote HTN and in the CKD patient, resistance. Sodium 247-253 renin Homo sapiens 114-119 25767289-2 2015 Increasing sodium intake is associated with increasing blood pressure, whereas low sodium intake results in increased renin and aldosterone levels. Sodium 83-89 renin Homo sapiens 118-123 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Sodium 15-21 renin Homo sapiens 71-76 24958786-1 2015 BACKGROUND: In cross-sectional studies, the aldosterone-to-renin ratio (ARR) has been reported to be associated with hypertension under conditions of higher sodium intake. Sodium 157-163 renin Homo sapiens 59-64 26028241-5 2015 It is thought that the renin-angiotensin system may play an important role in determining how much sodium the body expels or retains after salt intake is suddenly reduced or augmented. Sodium 99-105 renin Homo sapiens 23-28 25554067-5 2014 Increased distal sodium delivery may also act to suppress the intrarenal renin-angiotensin-aldosterone system, although systemic activity may be modestly increased due to osmotic diuresis. Sodium 17-23 renin Homo sapiens 73-78 25704353-4 2015 Calcineurin inhibitors, the most commonly used class of immunosuppressives, cause endothelial dysfunction, increase vascular tone, and sodium retention via the renin-angiotensin-aldosterone system resulting in systemic hypertension. Sodium 135-141 renin Homo sapiens 160-165 26024055-5 2015 Based largely on rodent studies, low-sodium diets have been associated with changes in glycemic control, energy metabolism, cardiovascular disease risk, cholesterol concentrations, inflammation, and functioning of the renin-angiotensin-aldosterone system. Sodium 37-43 renin Homo sapiens 218-223 25398734-3 2014 The role that modified sodium or potassium intake plays in influencing the renin-angiotensin system, arterial stiffness, and endothelial dysfunction remains of interest in current research. Sodium 23-29 renin Homo sapiens 75-80 24622156-10 2014 CONCLUSIONS: This study demonstrated the different responses of renin and aldosterone in SS and SR subjects based on dietary sodium intake whether or not they had hypertension. Sodium 125-131 renin Homo sapiens 64-69 25317016-0 2014 Urinary sodium excretion has positive correlation with activation of urinary renin angiotensin system and reactive oxygen species in hypertensive chronic kidney disease. Sodium 8-14 renin Homo sapiens 77-82 24840884-1 2014 PURPOSE OF REVIEW: The purpose of this review is to describe the renin-angiotensin-aldosterone system and its regulatory control of sodium, potassium, chloride, hydrogen ion, and water homeostasis through its effects on the expression and activity of distal renal tubular cotransporter proteins and to discuss the gene mutations encoding these structures that disturb the function of this system. Sodium 132-138 renin Homo sapiens 65-70 24944035-1 2014 The renin-angiotensin system has powerful effects in control of the blood pressure and sodium homeostasis. Sodium 87-93 renin Homo sapiens 4-9 24840297-1 2014 PURPOSE OF REVIEW: Sodium balance is primarily regulated through the renin-angiotensin-aldosterone system. Sodium 19-25 renin Homo sapiens 69-74 24622156-0 2014 The unique response of renin and aldosterone to dietary sodium intervention in sodium sensitivity. Sodium 56-62 renin Homo sapiens 23-28 24622156-0 2014 The unique response of renin and aldosterone to dietary sodium intervention in sodium sensitivity. Sodium 79-85 renin Homo sapiens 23-28 24622156-2 2014 The renin-angiotensin-aldosterone system plays a critical role in sodium handling and hypertension. Sodium 66-72 renin Homo sapiens 4-9 24622156-3 2014 We identified the specific responses of renin and aldosterone based on dietary sodium intake and revealed the relationship between these hormonal changes and dietary sodium intake in patients with SS. Sodium 79-85 renin Homo sapiens 40-45 25043079-0 2014 Effects of mildly increasing dialysis sodium removal on renin and sympathetic system in hemodialysis patients. Sodium 38-44 renin Homo sapiens 56-61 24581676-1 2014 In a meta-analysis that investigated the effects of dietary sodium restriction in diabetes nephropathy, although blood pressure fell, there were significant increases in plasma renin and aldosterone levels. Sodium 60-66 renin Homo sapiens 177-182 25043079-1 2014 BACKGROUND: It has been argued that the benefits of reducing sodium loading may be offset by increased activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. Sodium 61-67 renin Homo sapiens 121-126 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 renin Homo sapiens 79-84 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 renin Homo sapiens 251-256 23744888-5 2013 Sodium depletion and captopril led to activation and differentiation of these cells into renin-expressing cells in the adult kidney. Sodium 0-6 renin Homo sapiens 89-94 30546768-6 2013 It is known that the long-term usage of loop diuretics causes tolerance because it promotes sodium re-absorption through the proximal renal tubules by activating the renin-angiotensin-aldosterone system. Sodium 92-98 renin Homo sapiens 166-171 23136031-0 2013 The dual blockade of the renin-angiotensin system in hemodialysis patients requires decreased dialysate sodium concentration. Sodium 104-110 renin Homo sapiens 25-30 23136031-1 2013 PURPOSE: The study evaluated whether the dual blockade of the renin-angiotensin system may influence the sodium balance in hemodialysis. Sodium 105-111 renin Homo sapiens 62-67 23136031-9 2013 CONCLUSIONS: The dual blockade of the renin-angiotensin system affects sodium balance, increasing the sodium gradient, thus elevating thirst sensation and enhancing interdialytic weight gain. Sodium 71-77 renin Homo sapiens 38-43 23913386-1 2013 The renin-angiotensin-aldosterone system plays a key role in regulating blood pressure by maintaining vascular tone and the water/sodium balance. Sodium 130-136 renin Homo sapiens 4-9 23548411-0 2013 Renin-angiotensin system blockers may create more risk than reward for sodium-depleted cardiovascular patients with high plasma renin levels. Sodium 71-77 renin Homo sapiens 0-5 23548411-0 2013 Renin-angiotensin system blockers may create more risk than reward for sodium-depleted cardiovascular patients with high plasma renin levels. Sodium 71-77 renin Homo sapiens 128-133 23548411-5 2013 RESULTS: We showed (i) that PRA levels are usually medium to low in treated cardiovascular patients, but are sometimes abnormally high, (ii) that excessive sodium depletion can induce such high PRA levels, (iii) that the higher PRA patients exhibited evidence of sodium depletion: lower blood pressures, more frequent natriuretic drug usage, lower N-terminal pro b-type natriuretic peptide (NT-proBNP), and higher blood urea nitrogen and uric acid levels, with similar usage of renin-angiotensin blocking drugs. Sodium 156-162 renin Homo sapiens 478-483 23608658-0 2013 Effect of contrasted sodium diets on the pharmacokinetics and pharmacodynamic effects of renin-angiotensin system blockers. Sodium 21-27 renin Homo sapiens 89-94 23397215-3 2013 The characteristic low-renin, salt-sensitive hypertension of blacks is consistent with the kidney reabsorbing additional sodium (Na), which leads to an expanded plasma volume that drives the BP. Sodium 121-127 renin Homo sapiens 23-28 23608658-1 2013 Dietary sodium, the main determinant of the pharmacodynamic response to renin-angiotensin system blockade, influences the pharmacokinetics of various cardiovascular drugs. Sodium 8-14 renin Homo sapiens 72-77 23263240-10 2013 The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05). Sodium 9-15 renin Homo sapiens 53-58 23512453-0 2013 Sodium depletion in patients in clinical trials may account for the increased cardiovascular risk of dual blockade of the renin-angiotensin system. Sodium 0-6 renin Homo sapiens 122-127 23497963-1 2013 Ascites formation in patients with cirrhosis, portal hypertension, or both usually results from hyperdynamic circulatory dysfunction, where the retention of sodium and water is associated with the activation of the sympathetic and renin-angiotensin-aldosterone systems. Sodium 157-163 renin Homo sapiens 231-236 22990760-1 2013 Sustained stimulation of the intrarenal/intratubular renin-angiotensin system in a setting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, proliferation, fibrosis, and eventual renal injury. Sodium 163-169 renin Homo sapiens 53-58 23096366-3 2013 Under physiological conditions, renin secretion is determined mainly by sodium intake, but the specific pathways involved and the relations between them are not well defined. Sodium 72-78 renin Homo sapiens 32-37 23096366-4 2013 In animals, renin secretion is a log-linear function of sodium intake. Sodium 56-62 renin Homo sapiens 12-17 22990760-8 2013 Thus, increased collecting duct renin contributes to Ang II-dependent hypertension by augmenting distal nephron intratubular Ang II formation leading to sustained stimulation of sodium reabsorption and progression of hypertension. Sodium 178-184 renin Homo sapiens 32-37 22807466-8 2012 In a multivariable model, plasma renin showed a positive correlation with heart rate and male sex and a negative correlation with blood pressure, urinary sodium, glucose, and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) (adjusted R(2): 0.167, P< 0.001). Sodium 154-160 renin Homo sapiens 33-38 22899870-8 2012 Sodium restriction can lower BP and among patients with proteinuria can even enhance the anti-proteinuric effects of drugs that block the renin-angiotensin system. Sodium 0-6 renin Homo sapiens 138-143 22627176-2 2012 However, multiple randomized trials have also demonstrated that similar reductions in sodium increase plasma renin activity and aldosterone secretion, insulin resistance, sympathetic nerve activity, serum cholesterol, and triglyceride levels. Sodium 86-92 renin Homo sapiens 109-114 23012790-1 2012 While the circulating renin-angiotensin-aldosterone system(RAAS) plays an important role in the regulation of the sodium and extracellular fluid balance and blood pressure, the tissue RAAS has been reported to be involved in the pathophysiology of organ damage in patients with hypertension and diabetes. Sodium 114-120 renin Homo sapiens 22-27 22844565-2 2012 The purpose of this study was to compare the effect of sodium-restricted and unrestricted diets on plasma renin activity (PRA), renal blood flow (RBF) and ascites in patients with liver cirrhosis. Sodium 55-61 renin Homo sapiens 106-111 22361573-7 2012 CONCLUSIONS: The renin-angiotensin-aldosterone system of VLBW infants seems to be able, even immediately after birth, to respond to variations of plasma sodium concentrations; measurement of UAE constitutes an interesting method to determine aldosterone production, avoiding blood sampling in neonates so small and frail as VLBW infants. Sodium 153-159 renin Homo sapiens 17-22 22566498-6 2012 Also notable among the 273 polymorphisms was rs11649420 on chromosome 16 in the amiloride-sensitive sodium channel subunit SCNN1G involved in mediating renal sodium reabsorption and maintaining blood pressure when the renin-angiotensin system is inhibited by candesartan. Sodium 100-106 renin Homo sapiens 218-223 22639013-2 2012 However, multiple randomized trials have also demonstrated that similar reductions in sodium increase plasma renin activity and aldosterone secretion, insulin resistance, sympathetic nerve activity, serum cholesterol and triglyceride levels. Sodium 86-92 renin Homo sapiens 109-114 22068710-13 2012 CONCLUSIONS: Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride. Sodium 13-19 renin Homo sapiens 153-158 24713869-0 2012 Sodium handling is associated with liver function impairment and renin-aldosterone axis activity in patients with preascitic cirrhosis without hyponatremia. Sodium 0-6 renin Homo sapiens 65-70 22068710-12 2012 Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008). Sodium 0-6 renin Homo sapiens 54-59 24713869-3 2012 We aimed to investigate whether parameters of renal sodium handling (serum sodium, urinary sodium and fractional exertion of sodium (FeNa%) correlate with markers of liver function and renin-aldosterone axis activity in patients with preascitic cirrhosis without hyponatremia. Sodium 52-58 renin Homo sapiens 185-190 23316343-6 2012 Increased sodium concentration inside the brain activates epithelial sodium channels and the renin-angiotensin-aldosterone system in the brain. Sodium 10-16 renin Homo sapiens 93-98 21938070-0 2011 The plasma renin test reveals the contribution of body sodium-volume content (V) and renin-angiotensin (R) vasoconstriction to long-term blood pressure. Sodium 55-61 renin Homo sapiens 11-16 22089249-6 2012 RESULTS: As expected, blood pressure declined and measures of circulating renin-angiotensin-aldosterone system activity rose significantly with low-sodium diet. Sodium 148-154 renin Homo sapiens 74-79 21938070-5 2011 The low renin, sodium-volume dependent (V) form of essential hypertension occurs whenever body sodium content increases beyond the point where plasma renin-angiotensin vasoconstrictor activity is turned off. Sodium 15-21 renin Homo sapiens 8-13 21938070-5 2011 The low renin, sodium-volume dependent (V) form of essential hypertension occurs whenever body sodium content increases beyond the point where plasma renin-angiotensin vasoconstrictor activity is turned off. Sodium 15-21 renin Homo sapiens 150-155 21938070-5 2011 The low renin, sodium-volume dependent (V) form of essential hypertension occurs whenever body sodium content increases beyond the point where plasma renin-angiotensin vasoconstrictor activity is turned off. Sodium 95-101 renin Homo sapiens 8-13 21938070-6 2011 In contrast, medium to high renin (R) hypertension occurs when too much renin is secreted relative to the body sodium content. Sodium 111-117 renin Homo sapiens 28-33 21886976-2 2011 Sodium retention could be secondary to activation of renin-angiotensin-aldosterone axis or due to an intrinsic activation of Na(+)K(+) ATPase in the cortical collecting duct. Sodium 0-6 renin Homo sapiens 53-58 22000651-3 2011 Animal models have suggested a two-step pathogenesis by which uric acid initially activates the renin angiotensin system and suppresses nitric oxide, leading to uric acid-dependent increase in systemic vascular resistance, followed by a uric acid-mediated vasculopathy, involving renal afferent arterioles, resulting in a late sodium-sensitive hypertension. Sodium 327-333 renin Homo sapiens 96-101 22071811-13 2011 AUTHORS" CONCLUSIONS: Sodium reduction resulted in a 1% decrease in blood pressure in normotensives, a 3.5% decrease in hypertensives, a significant increase in plasma renin, plasma aldosterone, plasma adrenaline and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride. Sodium 22-28 renin Homo sapiens 168-173 20707915-3 2010 Previous research indicates that the FURIN gene may play a pivotal role in the renin-angiotensin system and maintaining the sodium-electrolyte balance. Sodium 124-130 renin Homo sapiens 79-84 21124331-11 2011 In conclusion, relative aldosterone excess or low-renin hypertension may have an important role in HBP hypertension in the general population with high sodium intake. Sodium 152-158 renin Homo sapiens 50-55 21595187-0 2011 [The role of renin-angiotensin-aldosterone system in salty taste and sodium intake regulation]. Sodium 69-75 renin Homo sapiens 13-18 21339086-1 2011 The increased activity of intrarenal renin-angiotensin system (RAS) in a setting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, proliferation, fibrosis and renal injury. Sodium 153-159 renin Homo sapiens 37-42 21941653-3 2011 The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. Sodium 20-26 renin Homo sapiens 151-156 21941653-3 2011 The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. Sodium 47-53 renin Homo sapiens 151-156 21468184-6 2009 Activation of sympathetic nervous system, renin-angiotensin-aldosterone system and non-osmotic vasopressin release stimulate the renal tubular reabsorption of sodium and water. Sodium 159-165 renin Homo sapiens 42-47 21462849-4 2010 Early studies in hypertension identified specific enzymes, channels and receptors implicating sodium handling in the regulation of blood pressure including genes involved with the renin-angiotensin-aldosterone system controlling blood pressure and salt-water homeostasis, proteins in hormonal regulation of blood pressure (enzymes and receptors of the mineralo- and glucocorticoid pathways) and proteins coded by genes involved in the structure and/or regulation of vascular tone (endothelins and their receptors). Sodium 94-100 renin Homo sapiens 180-185 19789444-15 2010 Excretion of an acute fluid load containing sodium and chloride may be dependent on a sustained suppression of the renin-angiotensin-aldosterone system rather than on natriuretic peptides. Sodium 44-50 renin Homo sapiens 115-120 20532698-5 2010 Activation of the sympathetic nervous system and the renin-angiotensin system, leading to renal sodium and water retention, links obesity with hypertension. Sodium 96-102 renin Homo sapiens 53-58 20671624-5 2010 Obesity increases renal sodium reabsorption by activating the renin-angiotensin and sympathetic nervous systems, and by altering intrarenal physical forces. Sodium 24-30 renin Homo sapiens 62-67 19593208-10 2009 CONCLUSION: The CYP2C9*3 allele was associated with lower activity of the renin-angiotensin-aldosterone system in hypertensive men, which may reflect a more efficient sodium reabsorption capacity. Sodium 167-173 renin Homo sapiens 74-79 19617274-2 2009 The sodium and water retention causes suppression of renin release. Sodium 4-10 renin Homo sapiens 53-58 20041594-2 2009 A dysregulated renin-angiotensin-aldosterone system may contribute to excess sodium retention and hypertension and may be activated in OSA. Sodium 77-83 renin Homo sapiens 15-20 19073901-12 2009 The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than beta1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion. Sodium 194-200 renin Homo sapiens 333-338 19255824-1 2009 BACKGROUND: The inhibition of the renin-angiotensin system in the diabetic condition was reported to enhance the sodium sensitivity of blood pressure. Sodium 113-119 renin Homo sapiens 34-39 19490286-3 2009 Obesity-induced hypertension has multiple potential etiologic pathways, the most well established being increased renal sodium reabsorption with impaired pressure natriuresis via (1) activation of the renin-angiotensin system, (2) stimulation of the sympathetic nervous system, and (3) altered intrarenal physical forces. Sodium 120-126 renin Homo sapiens 201-206 20046983-4 2009 This brief review is focused on recent evidence that inappropriate activation of renin in distal nephron segments, by acting on angiotensinogen generated in the proximal tubule cells and delivered to the distal nephron may contribute to increased distal intrarenal angiotensin II formation, sodium retention and development and progression of hypertension. Sodium 291-297 renin Homo sapiens 81-86 19542911-7 2009 This hyperactivation of the renin-angiotensin-aldosterone system was associated with hyponatremia and hyperkalemia in the newborn infants, and high urinary sodium loss, consistent with a partial aldosterone resistance at birth. Sodium 156-162 renin Homo sapiens 28-33 18572207-5 2008 Therefore, we hypothesised that renin-angiotensin system (RAS) function is altered by changes in sodium intake during pregnancy. Sodium 97-103 renin Homo sapiens 32-37 18851690-0 2008 Renin-angiotensin-aldosterone responsiveness to low sodium and blood pressure reactivity to angiotensin-II are unrelated to cholesteryl ester transfer protein mass in healthy subjects. Sodium 52-58 renin Homo sapiens 0-5 18851690-7 2008 No significant differences in (changes) in mean arterial pressure, aldosterone and active plasma renin concentration in response to low sodium were observed between the lowest and highest tertiles of CETP mass, HDL-C and apolipoprotein A-I. Sodium 136-142 renin Homo sapiens 97-102 18704622-1 2009 Interactions between the renin-angiotensin-aldosterone system and other mechanisms determining sodium balance are important in the pathophysiology of hypertension. Sodium 95-101 renin Homo sapiens 25-30 18704622-2 2009 Low-renin hypertension is a common type of resistant hypertension and is often associated with increased sodium retention. Sodium 105-111 renin Homo sapiens 4-9 19146798-8 2009 Furthermore, research using this technique indicates the effectiveness of renin-angiotensin-aldosterone system blockers in correcting impaired sodium regulation and consequent hypertension in these individuals. Sodium 143-149 renin Homo sapiens 74-79 18983442-9 2009 Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Sodium 160-166 renin Homo sapiens 7-12 18983442-9 2009 Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Sodium 160-166 renin Homo sapiens 80-85 18983442-12 2009 Recent results indicate that renal denervation reduces ABP and renin activity, and that sodium loading may decrease renin without changes in ABP, glomerular filtration rate or beta(1)-mediated nerve activity. Sodium 88-94 renin Homo sapiens 116-121 24692821-20 2008 Blockade of the renin-angiotensin system restored the normal pattern of renal response to high sodium intake in these women. Sodium 95-101 renin Homo sapiens 16-21 18700548-4 2008 Increased intra-cranial sodium ions are known to augment sympathetic nervous system activity via stimulation of epithelial sodium channels, mineralocorticoid receptors, the renin-angiotensin-aldosterone system and endogenous digitalislike factors in the brain. Sodium 24-30 renin Homo sapiens 173-178 17989136-0 2008 Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium. Sodium 70-76 renin Homo sapiens 29-34 18560669-4 2008 Hormonal mechanisms including the renin-angiotensin system, aldosterone, and vasopressin are involved in modifying fetal renal excretion, reabsorption of sodium and water, and regulation of vascular volume. Sodium 154-160 renin Homo sapiens 34-39 17989136-0 2008 Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium. Sodium 148-154 renin Homo sapiens 29-34 17447595-4 2007 Sodium retention leads to severe low renin hypertension. Sodium 0-6 renin Homo sapiens 37-42 17656065-5 2007 Moderate sodium restriction, possibly combined with diuretic therapy, helps to maximize the effect of renin-angiotensin inhibitors. Sodium 9-15 renin Homo sapiens 102-107 17554565-1 2007 Sodium retention and edema are common features of nephrotic syndrome that are classically attributed to hypovolemia and activation of the renin-angiotensin-aldosterone system. Sodium 0-6 renin Homo sapiens 138-143 17223989-9 2007 CONCLUSIONS: MC2R mutations should be considered in children who have primary adrenal failure with apparent mild disturbances in renin-sodium homeostasis. Sodium 135-141 renin Homo sapiens 129-134 17066056-4 2006 This Review focuses on the counter-regulation between the dopaminergic and renin-angiotensin systems in the renal proximal tubule, which is the site of about 70% of total renal sodium reabsorption. Sodium 177-183 renin Homo sapiens 75-80 17032723-4 2007 OBJECTIVES: This study examined the ratio of serum aldosterone to plasma renin activity as an index of sodium wasting in patients with 21 OHD CAH, heterozygotes, and normal individuals. Sodium 103-109 renin Homo sapiens 73-78 17060507-1 2006 We tested the hypothesis that changes in sodium intake modulate adipose-tissue renin-angiotensin and natriuretic peptide system gene expression in humans. Sodium 41-47 renin Homo sapiens 79-84 17060507-6 2006 With high-sodium intake, systemic renin activity and aldosterone levels were suppressed, angiotensin-converting enzyme activity did not change, and systemic levels of the atrial natriuretic peptide increased. Sodium 10-16 renin Homo sapiens 34-39 16585956-2 2006 In the kidney, renin secretion is tightly linked to sodium intake and renal perfusion pressure, reflecting the important role of the renin-angiotensin system (RAS) in controlling body fluid volume and blood pressure. Sodium 52-58 renin Homo sapiens 15-20 16772637-4 2006 In addition, sodium restriction generates other, sometimes undesirable effects, including increased insulin resistance, activation of the renin-angiotensin system, and increased sympathetic nerve activity. Sodium 13-19 renin Homo sapiens 138-143 19789728-1 2006 It is well recognized that the renin-angiotensin system plays an important role in the regulation of arterial pressure and sodium homeostasis. Sodium 123-129 renin Homo sapiens 31-36 16464787-11 2006 This is most likely a compensatory phenomenon in addition to the increase in the renin-angiotensin system to prevent excess loss of sodium and water. Sodium 132-138 renin Homo sapiens 81-86 16006463-2 2005 The renin-angiotensin system (RAS) is directly concerned with sodium and water homeostasis. Sodium 62-68 renin Homo sapiens 4-9 15716702-4 2005 A shift in sodium status modifies the activity of the renin-angiotensin-aldosterone system and the effects of ACEi, but its effects on angiotensin-(1-7) are unknown. Sodium 11-17 renin Homo sapiens 54-59 15854151-4 2005 In renal failure, a defect in renal sodium excretory function leads to an abnormal pressure natriuresis relationship and activation of the renin-angiotensin-aldosterone system, contributing to the development of hypertension and progression of kidney disease. Sodium 36-42 renin Homo sapiens 139-144 16169319-1 2005 BACKGROUND: Sodium retention and volume expansion, mediated in part by aldosterone, are prominent features in low-renin hypertension. Sodium 12-18 renin Homo sapiens 114-119 15361890-0 2005 Influence of dietary sodium on the renin-angiotensin-aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria. Sodium 21-27 renin Homo sapiens 35-40 15361890-9 2005 Thus, reduced modulation of renin activity in response to sodium restriction and an increased aldosterone on a high sodium diet appear to identify characteristics of hypertensive patients predisposed to abnormal cardiac remodelling. Sodium 58-64 renin Homo sapiens 28-33 16403686-6 2005 The diuretic-induced decrease in total body sodium activates the renin-angiotensin system, thus rendering blood pressure maintenance angiotensin II-dependent. Sodium 44-50 renin Homo sapiens 65-70 15586010-8 2005 This hypothesis is supported by recent data showing that sodium retention and hypertension can develop when the balance of production of these free radicals is tipped towards O2*-, such as in diabetes, atherosclerosis and renin-angiotensin-system activation. Sodium 57-63 renin Homo sapiens 222-227 15675318-1 2005 Clinical and laboratory experiments have demonstrated that arginine vasopressin (AVP), renin-aldosterone system and catecholamines play a crucial role in water and sodium retention in edematous diseases, including congestive heart failure, nephrotic syndrome and liver cirrhosis. Sodium 164-170 renin Homo sapiens 87-92 15675318-6 2005 Also, norepinephrine increases sodium reabsorption in proximal tubules, and in part augments renin-aldosterone system that increases sodium reabsorption in distal nephron. Sodium 133-139 renin Homo sapiens 93-98 15569339-7 2004 An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Sodium 24-30 renin Homo sapiens 115-120 15962610-5 2004 In 73 patients with a history of hypertension plasma renin activity was estimated in basal conditions and after stimulation by sodium restriction and upright position. Sodium 127-133 renin Homo sapiens 53-58 14660513-1 2004 Exposure to prolonged bed rest is known to induce changes in the renin-angiotensin-aldosterone system (RAAS) by way of posture, sodium and potassium balance, and stress, which may have serious consequences for patients. Sodium 128-134 renin Homo sapiens 65-70 15068965-2 2004 Sympathetic nervous and renin-angiotensin-aldosterone system activation appear to play an important role in the sodium and water retention, rightward shift in the pressure-natriuresis, and blood pressure elevation observed in obese individuals. Sodium 112-118 renin Homo sapiens 24-29 15586018-1 2005 PURPOSE OF REVIEW: The renin-angiotensin system is a coordinated hormonal cascade important to the regulation of the renal sodium excretion and blood pressure. Sodium 123-129 renin Homo sapiens 23-28 14718610-10 2004 With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. Sodium 5-11 renin Homo sapiens 141-146 14718610-10 2004 With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. Sodium 89-95 renin Homo sapiens 141-146 15529607-10 2004 CONCLUSIONS: Octreotide in a short infusion treatment induces an inhibitory effect on renin aldosterone secretion which may be responsible for the benefical effects on sodium excretion. Sodium 168-174 renin Homo sapiens 86-91 14745661-2 2004 Approximately one third of these patients have elevated blood pressure due to increased sodium and water retention by the kidney resulting in suppressed plasma renin and aldosterone concentrations with high urinary potassium excretion and low plasma potassium levels. Sodium 88-94 renin Homo sapiens 160-165 15055250-0 2004 Blunted response of the renin-angiotensin system and nitric oxide synthesis related to sodium sensitivity in immunoglobulin A nephropathy. Sodium 87-93 renin Homo sapiens 24-29 15055250-7 2004 Changes in plasma renin activity and serum aldosterone during sodium restriction were greater in the low-index group than in the high-index group. Sodium 62-68 renin Homo sapiens 18-23 15055250-9 2004 These results indicate that impairment of NO synthesis and a blunted response of the renin-angiotensin system are attributable to the altered sodium sensitivity of blood pressure in patients with immunoglobulin A nephropathy. Sodium 142-148 renin Homo sapiens 85-90 15030296-6 2003 For example, the compensatory rise in renin secretion induced by sodium depletion may become the predominant factor sustaining high blood pressure. Sodium 65-71 renin Homo sapiens 38-43 12929469-6 2003 For example, the compensatory increase in renin secretion induced by sodium depletion may become the predominant factor sustaining high blood pressure. Sodium 69-75 renin Homo sapiens 42-47 12929469-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1 receptor blocker, makes this compensatory hyper-reninaemia ineffective and allows maximum benefit from sodium depletion. Sodium 197-203 renin Homo sapiens 29-34 12745204-0 2003 Relevance of the plasma renin hormonal control system that regulates blood pressure and sodium balance for correctly treating hypertension and for evaluating ALLHAT. Sodium 88-94 renin Homo sapiens 24-29 14551679-10 2003 Patients with PAC/renin activity less than 2 had higher total volume of infused fluid, serum creatinine level, and fractional excretion of sodium values; aldosterone and serum creatinine were negatively correlated. Sodium 139-145 renin Homo sapiens 18-23 14508195-1 2003 BACKGROUND: The prevailing sodium intake and renin-angiotensin system status influence the blood pressure response to an angiotensin II type 1 (AT1) receptor antagonist or an angiotensin I converting enzyme inhibitor, which is known to be reinforced by a low sodium intake or administration of a diuretic. Sodium 259-265 renin Homo sapiens 45-50 12927775-6 2003 This led to the discovery of aliskiren, a highly potent and selective inhibitor of human renin in vitro, and in vivo; once-daily oral doses of aliskiren inhibit renin and lower blood pressure in sodium-depleted marmosets and hypertensive human patients. Sodium 195-201 renin Homo sapiens 89-94 15030296-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1-receptor blocker, makes this compensatory hyper-reninemia ineffective and allows maximum benefit from sodium depletion. Sodium 196-202 renin Homo sapiens 29-34 12492779-1 2003 AIM: During heart failure (HF), excess sodium retention is triggered by increased plasma renin-angiotensin-aldosterone activity and increased basal sympathetic nerve discharge (SND). Sodium 39-45 renin Homo sapiens 89-94 12569273-0 2003 Reduced activity of the kallikrein-kinin system predominates over renin-angiotensin system overactivity in all conditions of sodium balance in essential hypertensives and family-related hypertension. Sodium 125-131 renin Homo sapiens 66-71 12589181-5 2003 Obesity increases renal sodium reabsorption by activating the renin-angiotensin and sympathetic nervous systems, and by altering intrarenal physical forces. Sodium 24-30 renin Homo sapiens 62-67 12419174-4 2002 Moreover, sodium depletion has multiple other effects including activation of the renin-angiotensin system and the sympathetic nervous system, and increase in insulin resistance. Sodium 10-16 renin Homo sapiens 82-87 12413503-0 2002 Serum to urinary sodium concentration ratio is an estimate of plasma renin activity in congestive heart failure. Sodium 17-23 renin Homo sapiens 69-74 11790293-3 2002 The importance of the renin-angiotensin system in controlling sodium homeostasis and vascular resistance is well established, however, in the past decade, much attention has been focused on the importance of angiotensin II as a regulator of microvessel density, acting through the AT1 and AT2 receptors. Sodium 62-68 renin Homo sapiens 22-27 12174326-10 2002 Finally, increased renal tubular reabsorption of sodium may also occur, caused by an increased renal sympathetic nerve activity, the direct effect of insulin, hyperactivity of the renin-angiotensin system and possibly by an alteration of intrarenal physical forces. Sodium 49-55 renin Homo sapiens 180-185 12215953-5 2002 As a consequence, activation of sodium- and volume-retaining neurohumoral systems such as the renin-angiotensin-aldosterone system and the sympathetic nervous system and a non-osmotic release of arginine-vasopressin can be observed. Sodium 32-38 renin Homo sapiens 94-99 12357279-7 2002 It is evident from experimental studies that an elevation in dietary sodium intake during the growing phase heightens neural control of blood pressure and the kidney partly due to an enhanced role of the brain renin-angiotensin system. Sodium 69-75 renin Homo sapiens 210-215 11875587-2 2002 The ubiquitous involvement of the renin-angiotensin-aldosterone system, originally conceived as an axis of sodium and fluid metabolism in inflammation, thrombosis and cardiac and smooth muscle hypertrophy, is a major factor in disease progression for conditions as diverse as hypertension, heart failure, coronary artery disease and diabetes. Sodium 107-113 renin Homo sapiens 34-39 11967726-1 2002 A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Sodium 104-110 renin Homo sapiens 2-7 11847182-0 2002 Low-renin hypertension, altered sodium homeostasis, and an alpha-adducin polymorphism. Sodium 32-38 renin Homo sapiens 4-9 11824860-1 2002 Salt-sensitive persons have lower plasma renin activity than salt-resistant persons and their plasma renin activity increases less with a low sodium diet or volume depletion, compared to salt-resistant individuals. Sodium 142-148 renin Homo sapiens 101-106 11882573-7 2002 Plasma renin activity and blood pressure response to diuretic treatment, on the other hand, showed a weaker association with the sodium transport rate. Sodium 129-135 renin Homo sapiens 7-12 11963285-12 2002 CONCLUSIONS: Our results show that intensive vasodilator therapy in patients with severe HF improves hemodynamic parameters and causes activation of renin-angiotensin-aldosterone and adrenergic systems, resulting in sodium retention. Sodium 216-222 renin Homo sapiens 149-154 11824860-12 2002 These findings point to an intrinsic difference in the regulation of renin release between salt-sensitive and salt-resistant subjects that may account for the different BP responses to changes in dietary sodium intake. Sodium 204-210 renin Homo sapiens 69-74 12036386-1 2002 The renin-angiotensin system exerts a cardinal role in the maintenance of blood pressure and in the regulation of water and sodium excretion through its multiple effects on the vasculature, the kidneys, the heart, the adrenal glands and the brain. Sodium 124-130 renin Homo sapiens 4-9 12036388-1 2002 The octapeptide angiotensin II (Ang II), the potent effector molecule of the renin-angiotensin-aldosterone system (RAAS), is involved in the control of blood pressure, cardiac and vascular function as well as sodium and water homeostasis. Sodium 209-215 renin Homo sapiens 77-82 11709521-6 2001 RESULTS: The daily diet of 200 mmol of sodium resulted in weight gain and a positive sodium balance for three weeks, associated with significant suppression of plasma renin activity and aldosterone levels, and a significant rise in plasma atrial natriuretic peptide levels (p<0.05). Sodium 39-45 renin Homo sapiens 167-172 11641319-2 2001 A coherent picture is emerging, with the final pathway of these mechanisms converging on the renin-angiotensin system in the presence of a positive sodium balance and responsible for arteriolar resistance and responsiveness to pressor agents. Sodium 148-154 renin Homo sapiens 93-98 11719734-0 2001 Low sodium and furosemide-induced stimulation of the renin system in man is mediated by cyclooxygenase 2. Sodium 4-10 renin Homo sapiens 53-58 11719734-3 2001 Plasma renin activity increased 2 to 3 times over baseline with a low-sodium diet and 5 times over baseline 30 minutes after intravenous furosemide; it was still elevated nearly 5 times on day 9. Sodium 70-76 renin Homo sapiens 7-12 11719734-7 2001 We have concluded that low-sodium and furosemide-stimulated renin and aldosterone secretion is completely blocked in healthy volunteers during COX-2 inhibition with rofecoxib, suggesting that intact COX-2 is of major importance for stimulation of the renin system under these conditions in man. Sodium 27-33 renin Homo sapiens 60-65 11710792-13 2001 Also in hypothyroid patients the application of a low sodium diet led to a lower increase in plasma renin activity in subjects with salt-sensitive BP than in individuals with salt-resistant BP. Sodium 54-60 renin Homo sapiens 100-105 11532707-8 2001 Sodium-retaining endocrine systems, such as renin-aldosterone and catecholamines, are much more activated during microG than on Earth. Sodium 0-6 renin Homo sapiens 44-49 11496053-2 2001 Cyclooxygenase-2 regulates renin-angiotensin secretion, and thereby glomerular filtration rate and sodium homeostasis. Sodium 99-105 renin Homo sapiens 27-32 11458030-5 2001 Applying these insights to the far more common disorder of low renin hypertension may shed new light on the underlying pathophysiology of this common form of human hypertension, and more clearly define the interactions of dietary constituents such as sodium and potassium in the regulation of blood pressure. Sodium 251-257 renin Homo sapiens 63-68 11318932-4 2001 The renin-angiotensin system plays a central role in this response and is balanced by developmental changes in the renal response to atrial natriuretic peptide, all of which contribute to sodium conservation. Sodium 188-194 renin Homo sapiens 4-9 11458695-8 2001 The responses to central administration of angiotensin II type AT1 receptor antagonists, into the ventricular system or microinjected into the rostral ventrolateral medulla, are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 renin Homo sapiens 218-223 11299228-0 2001 Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans. Sodium 75-81 renin Homo sapiens 43-48 11299228-5 2001 The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 +/- 64 vs. 10 +/- 9 meq/24 h, P < 0.001; losartan: 141 +/- 56 vs. 14 +/- 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 +/- 0.5 vs. 5.0 +/- 2.5 ng x ml(-1) x h(-1), P < 0.001; losartan: 3.8 +/- 7.2 vs. 19.1 +/- 11.2 ng x ml(-1) x h(-1), P = 0.006) in both the losartan and placebo groups. Sodium 8-14 renin Homo sapiens 217-222 11515306-2 2001 Six NHS, acting in CHF, have presently been identified: three of them induce vasoconstriction and sodium retention (sympathetic nervous systems, renin-angiotensin-aldosterone system and arginine-vasopressine system); the remaining three offset or balance the former ones, acting, therefore as "counterregulators" (prostaglandins--PGE2 and PGI2--, dopaminergic system and atrial natriuretic factor). Sodium 98-104 renin Homo sapiens 145-150