PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26667412-4 2016 Signaling through dopamine D1 receptor and angiotensin II type I receptor (AT1R) reciprocally modulates renal sodium excretion and blood pressure. Sodium 110-116 angiotensinogen Homo sapiens 43-57 26116142-6 2015 After adjustment for gestational age, urinary angiotensinogen level correlated with urinary fractional excretion of sodium and urinary levels of cystatin-C and alpha1-microglobulin. Sodium 116-122 angiotensinogen Homo sapiens 46-61 26420482-7 2015 We further observed that the mutation N111(3.35)A in the putative sodium-binding site affects binding of the endogenous peptide agonist angiotensin II but not the beta-arrestin-biased peptide TRV120027. Sodium 66-72 angiotensinogen Homo sapiens 136-150 26486596-11 2015 Urine sodium was associated with low and normal angiotensin II levels (P value 0.007). Sodium 6-12 angiotensinogen Homo sapiens 48-62 24049115-9 2013 Hence, some of the same circulating hormones controlling ENaC expression in kidney, such as angiotensin II and atrial natriuretic peptide, may coordinate ENaC expression in sensory CVO neurons and could potentially orchestrate sodium appetite, osmoregulation, and vasomotor sympathetic drive. Sodium 227-233 angiotensinogen Homo sapiens 92-106 25858030-2 2015 The sympathetic control of renal sodium tubular reabsorption is dependent on activation of the intrarenal renin-angiotensin system and activation of the angiotensin II type 1 (AT1 ) receptor by angiotensin II. Sodium 33-39 angiotensinogen Homo sapiens 153-167 25858030-6 2015 In this short review, the crosstalk between intrarenal angiotensin II and renal nerve activity and its effect on sodium reabsorption is addressed. Sodium 113-119 angiotensinogen Homo sapiens 55-69 25858030-11 2015 Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS. Sodium 229-235 angiotensinogen Homo sapiens 158-164 25374825-4 2014 AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Sodium 27-33 angiotensinogen Homo sapiens 0-5 25374825-4 2014 AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Sodium 61-67 angiotensinogen Homo sapiens 0-5 25317016-6 2014 During the 16-week follow-up period, an increase in urinary sodium excretion predicted an increase in urinary angiotensinogen excretion. Sodium 60-66 angiotensinogen Homo sapiens 110-125 25024004-5 2014 Essentially, T-lymphocytes determine an increase in angiotensin ii production which raises sodium and water retention. Sodium 91-97 angiotensinogen Homo sapiens 52-66 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 78-84 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 166-172 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 166-172 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 angiotensinogen Homo sapiens 188-202 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 angiotensinogen Homo sapiens 204-210 25019012-7 2013 The augmented intratubular Ang II concentrations together with elevated renal interstitial Ang II concentrations contribute to sustained stimulation of sodium reabsorption, vasoconstriction, development of hypertension, and progressive renal injury and fibrosis. Sodium 152-158 angiotensinogen Homo sapiens 27-33 25019012-7 2013 The augmented intratubular Ang II concentrations together with elevated renal interstitial Ang II concentrations contribute to sustained stimulation of sodium reabsorption, vasoconstriction, development of hypertension, and progressive renal injury and fibrosis. Sodium 152-158 angiotensinogen Homo sapiens 91-97 25987608-2 2015 The increased intrarenal angiotensin II (Ang II) elicits renal vasoconstriction and enhanced tubular sodium reabsorption in proximal and distal nephron segments. Sodium 101-107 angiotensinogen Homo sapiens 25-39 25987608-2 2015 The increased intrarenal angiotensin II (Ang II) elicits renal vasoconstriction and enhanced tubular sodium reabsorption in proximal and distal nephron segments. Sodium 101-107 angiotensinogen Homo sapiens 41-47 25987608-4 2015 The increased AGT formation and secretion into the proximal tubular lumen leads to local formation of Ang II, which stimulates proximal transporters such as the sodium/hydrogen exchanger. Sodium 161-167 angiotensinogen Homo sapiens 14-17 25987608-4 2015 The increased AGT formation and secretion into the proximal tubular lumen leads to local formation of Ang II, which stimulates proximal transporters such as the sodium/hydrogen exchanger. Sodium 161-167 angiotensinogen Homo sapiens 102-108 25987608-6 2015 There is also increased Ang II concentration in distal nephron with stimulation of distal sodium transport. Sodium 90-96 angiotensinogen Homo sapiens 24-30 25858030-0 2015 Crosstalk between the renal sympathetic nerve and intrarenal angiotensin II modulates proximal tubular sodium reabsorption. Sodium 103-109 angiotensinogen Homo sapiens 61-75 25681793-1 2015 Angiotensin II (AngII) is an octapeptide hormone that plays a central role in regulation of sodium balance, plasma volume, and blood pressure. Sodium 92-98 angiotensinogen Homo sapiens 0-14 25681793-1 2015 Angiotensin II (AngII) is an octapeptide hormone that plays a central role in regulation of sodium balance, plasma volume, and blood pressure. Sodium 92-98 angiotensinogen Homo sapiens 16-21 24310820-5 2014 For example, the recent discoveries that NCC is activated by angiotensin II but inhibited by dietary potassium shed light on how the kidney handles sodium during hypovolemia (high angiotensin II) and hyperkalemia. Sodium 148-154 angiotensinogen Homo sapiens 180-194 24310820-6 2014 The additive effect of angiotensin II and aldosterone maximizes sodium reabsorption during hypovolemia, whereas the inhibitory effect of potassium on NCC increases delivery of sodium to the potassium-secreting portion of the nephron. Sodium 64-70 angiotensinogen Homo sapiens 23-37 26105897-14 2013 Angiotensin II promotes sodium retention at the proximal tubule independently of aldosterone. Sodium 24-30 angiotensinogen Homo sapiens 0-14 23263240-10 2013 The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05). Sodium 9-15 angiotensinogen Homo sapiens 82-96 23097467-4 2013 Dopamine and angiotensin II are the two key renal factors that, via acting on their receptors and counterregulating each other"s function, maintain water and sodium balance. Sodium 158-164 angiotensinogen Homo sapiens 13-27 23259473-2 2013 Pathophysiological effects mediated via angiotensin II (Ang II) are well established in regulation of blood pressure, cardiac and vascular remodeling, and renal sodium handling, which lead to disorders such as hypertension and associated end-organ damage, atherosclerosis and heart failure. Sodium 161-167 angiotensinogen Homo sapiens 40-54 23165113-0 2013 Effects of angiotensin II on kinase-mediated sodium and potassium transport in the distal nephron. Sodium 45-51 angiotensinogen Homo sapiens 11-25 23165113-1 2013 PURPOSE OF REVIEW: The aim is to review the recently reported effects of angiotensin II (Ang II) on sodium and potassium transport in the aldosterone-sensitive distal nephron, including the signaling pathways between receptor and transporter, and the (patho)physiological implications of these findings. Sodium 100-106 angiotensinogen Homo sapiens 73-87 23165113-1 2013 PURPOSE OF REVIEW: The aim is to review the recently reported effects of angiotensin II (Ang II) on sodium and potassium transport in the aldosterone-sensitive distal nephron, including the signaling pathways between receptor and transporter, and the (patho)physiological implications of these findings. Sodium 100-106 angiotensinogen Homo sapiens 89-95 23165113-8 2013 SUMMARY: The effects of Ang II on NCC, ENaC, and ROMK help explain the renal response to hypovolemia which is to conserve both sodium and potassium. Sodium 127-133 angiotensinogen Homo sapiens 24-30 23259473-2 2013 Pathophysiological effects mediated via angiotensin II (Ang II) are well established in regulation of blood pressure, cardiac and vascular remodeling, and renal sodium handling, which lead to disorders such as hypertension and associated end-organ damage, atherosclerosis and heart failure. Sodium 161-167 angiotensinogen Homo sapiens 56-62 22820370-9 2012 SUMMARY: Modulation of WNK4 activity by AngII underlies the effects of AngII on NCC activity and this is probably important for the stimulation of renal sodium retention, as well as for the prevention of potassium loss, during hypovolemia. Sodium 153-159 angiotensinogen Homo sapiens 40-45 22871893-7 2012 In addition to age and sex, 24-h urinary sodium excretion was an independent determinant of urinary angiotensinogen-to-creatinine ratio (P = 0.0008). Sodium 41-47 angiotensinogen Homo sapiens 100-115 22871893-8 2012 Urinary angiotensinogen-to-creatinine ratio was 34% (P = 0.04) and 82% (P <= 0.0001) higher in tertiles 2 and 3 of 24-h urinary sodium excretion, respectively, than in tertile 1. Sodium 131-137 angiotensinogen Homo sapiens 8-23 22871893-10 2012 CONCLUSION: Urinary angiotensinogen excretion is higher with greater urinary sodium excretion, and is associated with clinic and ambulatory BP. Sodium 77-83 angiotensinogen Homo sapiens 20-35 23165302-7 2013 Finally, a role of angiotensin II in sodium and potassium handling in the distal nephron has been identified. Sodium 37-43 angiotensinogen Homo sapiens 19-33 22820370-9 2012 SUMMARY: Modulation of WNK4 activity by AngII underlies the effects of AngII on NCC activity and this is probably important for the stimulation of renal sodium retention, as well as for the prevention of potassium loss, during hypovolemia. Sodium 153-159 angiotensinogen Homo sapiens 71-76 22573118-0 2012 Proximal tubular angiotensinogen in renal biopsy suggests nondipper BP rhythm accompanied by enhanced tubular sodium reabsorption. Sodium 110-116 angiotensinogen Homo sapiens 17-32 22573118-6 2012 CONCLUSION: Tubular sodium reabsorption is stimulated by intrarenal angiotensin II, as indicated by PT-AGT, and contributes to the genesis of the nondipper BP rhythm. Sodium 20-26 angiotensinogen Homo sapiens 68-82 21849491-2 2011 In the current studies, we used a kidney cross-transplantation strategy to determine whether increased sodium reabsorption by AT(1) receptors in the kidney mediates the chronic hypertensive response to angiotensin II. Sodium 103-109 angiotensinogen Homo sapiens 202-216 21088669-7 2011 RESULTS: The effect of sodium intake on BP differed by genotype at the angiotensinogen, beta2-adrenergic receptor, and kallikrein loci. Sodium 23-29 angiotensinogen Homo sapiens 71-86 21670416-7 2011 The sodium sensitivity index in our patients positively correlated with the glomerulosclerosis score (r=0.43; P=0.008) and changes in logarithmic urinary angiotensinogen:creatinine ratio (r=0.37; P=0.017) but not with changes in urinary protein excretion (r=0.18; P=0.49). Sodium 4-10 angiotensinogen Homo sapiens 154-169 21245763-4 2011 Hypertensive stimuli such as the effector molecule of the renin-angiotensin system, angiotensin II, not only regulate vascular tone and sodium balance, but also activate immune cells and promote cell infiltration into target organs. Sodium 136-142 angiotensinogen Homo sapiens 58-98 20486869-2 2010 The final step in RAAS stimulation is aldosterone secretion by angiotensin II, which leads to increased renal tubular sodium absorption and potassium secretion. Sodium 118-124 angiotensinogen Homo sapiens 63-77 20486869-5 2010 With such combinations, while ARB inhibits the vasoconstricting action and aldosterone-secreting effects of angiotensin II, hydrochlorothiazide affects the renal tubular mechanisms of electrolyte reabsorption and directly increases excretion of sodium and chloride in the distal tubule, and promotes water excretion. Sodium 245-251 angiotensinogen Homo sapiens 108-122 20683640-11 2010 VALIDATION: (1) model BP, PRA and [Ang II] are within reported ranges, and respond physiologically to sodium intake; (2) short-term Ang II infusion induces reported rise in BP and PRA. Sodium 102-108 angiotensinogen Homo sapiens 35-41 20683640-11 2010 VALIDATION: (1) model BP, PRA and [Ang II] are within reported ranges, and respond physiologically to sodium intake; (2) short-term Ang II infusion induces reported rise in BP and PRA. Sodium 102-108 angiotensinogen Homo sapiens 132-138 19909757-3 2010 Variations in the sodium content of the diet, through hormonal mediators such as dopamine and angiotensin II, modulate renal tubule Na(+),K(+)-ATPase activity. Sodium 18-24 angiotensinogen Homo sapiens 94-108 20308605-8 2010 Thus, women with a history of hypertensive pregnancy demonstrated salt sensitivity of blood pressure and had increased pressor, adrenal, and soluble fms-like tyrosine kinase 1 responses to infused angiotensin II in low-sodium balance. Sodium 219-225 angiotensinogen Homo sapiens 197-211 21118180-2 2010 Vasoconstriction and sodium and water retention, due to angiotensin II and aldosterone promote atherosclerotic processes. Sodium 21-27 angiotensinogen Homo sapiens 56-70 20216091-0 2010 A mechanism for salt-sensitive hypertension: abnormal dietary sodium-mediated vascular response to angiotensin-II. Sodium 62-68 angiotensinogen Homo sapiens 99-113 20484892-2 2010 The kidney contains all elements of the RAAS, and intrarenal formation of angiotensin II not only controls glomerular hemodynamics and tubule sodium transport, but also activates a number of inflammatory and fibrotic pathways. Sodium 142-148 angiotensinogen Homo sapiens 74-88 19770777-7 2010 Sodium depletion enhances associations between AGT SNPs and plasma AGT. Sodium 0-6 angiotensinogen Homo sapiens 47-50 19770777-7 2010 Sodium depletion enhances associations between AGT SNPs and plasma AGT. Sodium 0-6 angiotensinogen Homo sapiens 67-70 19770777-12 2010 By demonstrating the dependence of AGT associations on sodium depletion status, it helps to explain previous conflicting association results. Sodium 55-61 angiotensinogen Homo sapiens 35-38 18701625-3 2008 We have previously demonstrated that the level of intracellular sodium concentration modulates the regulation of Na-K-ATPase activity by angiotensin II and dopamine. Sodium 64-70 angiotensinogen Homo sapiens 137-151 19563532-0 2009 Pals-associated tight junction protein functionally links dopamine and angiotensin II to the regulation of sodium transport in renal epithelial cells. Sodium 107-113 angiotensinogen Homo sapiens 71-85 19546583-1 2009 BACKGROUND/AIMS: Angiotensin II promotes sodium retention and influences the central regulation of fluid intake. Sodium 41-47 angiotensinogen Homo sapiens 17-31 18818245-1 2008 Angiotensin II (ANGII) plays a central role in the enhanced sodium reabsorption in early type 1 diabetes in man and in streptozotocin-induced (STZ) diabetic rats. Sodium 60-66 angiotensinogen Homo sapiens 0-14 18818245-1 2008 Angiotensin II (ANGII) plays a central role in the enhanced sodium reabsorption in early type 1 diabetes in man and in streptozotocin-induced (STZ) diabetic rats. Sodium 60-66 angiotensinogen Homo sapiens 16-21 18851690-4 2008 Blood pressure response to incremental angiotensin-II infusion was assessed in 34 subjects during liberal sodium diet. Sodium 106-112 angiotensinogen Homo sapiens 39-53 18689375-0 2008 Blood pressure and interactions between the angiotensin polymorphism AGT M235T and sodium intake: a cross-sectional population study. Sodium 83-89 angiotensinogen Homo sapiens 69-72 18689375-1 2008 BACKGROUND: Intervention studies have indicated an interaction between the blood pressure response to a low-sodium or a low-fat and high-fruit and -vegetable diet and the angiotensinogen gene (AGT) polymorphisms G-6A and M235T. Sodium 108-114 angiotensinogen Homo sapiens 171-186 18689375-1 2008 BACKGROUND: Intervention studies have indicated an interaction between the blood pressure response to a low-sodium or a low-fat and high-fruit and -vegetable diet and the angiotensinogen gene (AGT) polymorphisms G-6A and M235T. Sodium 108-114 angiotensinogen Homo sapiens 193-196 20641953-3 2004 Angiotensin II also stimulates the production of aldosterone from the adrenal glands, which promotes retention of sodium and water. Sodium 114-120 angiotensinogen Homo sapiens 0-14 18551010-4 2008 DESIGN AND METHODS: Three hundred fifteen participants had renal plasma flow response to subpressor doses of angiotensin II (3 ng/kg/min) measured by para-aminohippuric acid clearance in high-sodium balance. Sodium 192-198 angiotensinogen Homo sapiens 109-123 20641324-3 2004 Angiotensin II also stimulates the production of aldosterone from the adrenal glands that promotes sodium and water retention. Sodium 99-105 angiotensinogen Homo sapiens 0-14 18238849-0 2008 The role of SGK-1 in angiotensin II-mediated sodium reabsorption in human proximal tubular cells. Sodium 45-51 angiotensinogen Homo sapiens 21-35 18238849-1 2008 BACKGROUND: The role of angiotensin II (Ang II) in mediating excessive sodium reabsorption in diabetic nephropathy is recognized. Sodium 71-77 angiotensinogen Homo sapiens 24-38 18238849-1 2008 BACKGROUND: The role of angiotensin II (Ang II) in mediating excessive sodium reabsorption in diabetic nephropathy is recognized. Sodium 71-77 angiotensinogen Homo sapiens 40-46 18238849-8 2008 SGK-1 was silenced in the PTCs using small interfering RNA to determine the role of SGK-1 in mediating Ang II-induced increases in NHE3-mediated sodium uptake. Sodium 145-151 angiotensinogen Homo sapiens 103-109 18238849-13 2008 CONCLUSION: These data suggest that increased sodium reabsorption in renal proximal tubular cells considered to be due to Ang II in diabetes mellitus is mediated through SGK-1 expression. Sodium 46-52 angiotensinogen Homo sapiens 122-128 18219299-0 2008 Renal response to angiotensin II is blunted in sodium-sensitive normotensive men. Sodium 47-53 angiotensinogen Homo sapiens 18-32 18460877-12 2008 It is hypothesized that this is caused by sodium retention during the day mediated by renal nerve sympathetic activity which together with angiotensin II acts on the kidney to increase tubular sodium reabsorption either directly or by reducing daytime glomerular filtration rate. Sodium 193-199 angiotensinogen Homo sapiens 139-153 17487823-1 2007 Angiotensin II (Ang II) has powerful sodium-retaining, growth-promoting and pro- inflammatory properties in addition to its physiological role in maintaining body salt and fluid balance and blood pressure homeostasis. Sodium 37-43 angiotensinogen Homo sapiens 0-22 17931588-2 2007 High levels of angiotensin II may be responsible for hypertension and heart failure because they increase systemic vascular resistance, arterial pressure, and sodium and fluid retention. Sodium 159-165 angiotensinogen Homo sapiens 15-29 17895315-7 2007 RESULTS: In low-sodium balance, the increases in systolic and diastolic BP in response to infused AngII were blunted with increased serum progesterone concentrations (P < 0.05). Sodium 16-22 angiotensinogen Homo sapiens 98-103 17895315-13 2007 CONCLUSIONS: In postmenopausal women in low-sodium balance, the pressor and renovascular responses to AngII are blunted with increased endogenous progesterone concentrations. Sodium 44-50 angiotensinogen Homo sapiens 102-107 17665974-4 2007 Tubular NADPH oxidase stimulated by angiotensin II or aldosterone contributes to sodium retention and to tubulointerstitial damage. Sodium 81-87 angiotensinogen Homo sapiens 36-50 17587492-2 2007 Angiotensin II (Ang II) is a potent growth factor for glomerulosa cells, appearing as a proliferative factor in vivo, under sodium-deficient diet conditions, as well as in vitro, in studies conducted with whole zona glomerulosa. Sodium 124-130 angiotensinogen Homo sapiens 0-14 17587492-2 2007 Angiotensin II (Ang II) is a potent growth factor for glomerulosa cells, appearing as a proliferative factor in vivo, under sodium-deficient diet conditions, as well as in vitro, in studies conducted with whole zona glomerulosa. Sodium 124-130 angiotensinogen Homo sapiens 16-22 17519130-4 2007 Ang II signaling is integrated with sodium-sensitive neurons in the SFO and/or organum vasculosum of the lamina terminalis (OVLT) and drives sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) via the paraventricular nucleus (PVN). Sodium 36-42 angiotensinogen Homo sapiens 0-6 16890144-0 2006 Dietary sodium intake modulates myocardial relaxation responsiveness to angiotensin II. Sodium 8-14 angiotensinogen Homo sapiens 72-86 16868049-7 2006 RESULTS: In high-sodium balance, urinary aldosterone, basal serum aldosterone, and serum aldosterone response to infused AngII were significantly greater (P < 0.05) in the luteal vs. follicular phase. Sodium 17-23 angiotensinogen Homo sapiens 121-126 17969373-2 2007 The effect of angiotensin II is mediated via the angiotensin type I receptor (AT1 ) resulting in vasoconstriction, sodium retention and myocyte growth changes. Sodium 115-121 angiotensinogen Homo sapiens 14-28 16890144-1 2006 Dietary sodium alters renovascular responsiveness to angiotensin II (Ang II) in normal subjects. Sodium 8-14 angiotensinogen Homo sapiens 53-67 16890144-1 2006 Dietary sodium alters renovascular responsiveness to angiotensin II (Ang II) in normal subjects. Sodium 8-14 angiotensinogen Homo sapiens 69-75 16890144-7 2006 Dietary sodium significantly modulated E" and RBF responsiveness to Ang II infusion in like manner. Sodium 8-14 angiotensinogen Homo sapiens 68-74 16890144-9 2006 The authors describe for the first time that dietary sodium modulates myocardial relaxation and responsiveness to Ang II. Sodium 53-59 angiotensinogen Homo sapiens 114-120 16890144-11 2006 Ang II may play a role in the interaction between dietary sodium and myocardial relaxation. Sodium 58-64 angiotensinogen Homo sapiens 0-6 16611713-8 2006 These data highlight the critical role of MR in the maintenance of salt homeostasis early in life and illuminate the sodium dependence of pathologic effects of renin and angiotensin II. Sodium 117-123 angiotensinogen Homo sapiens 170-184 16142301-1 2005 Angiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. Sodium 87-93 angiotensinogen Homo sapiens 0-14 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensinogen Homo sapiens 0-14 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensinogen Homo sapiens 16-22 16601568-2 2006 RESULTS: AT1-receptor activation by angiotensin II is not only involved in the regulation of blood pressure, water and sodium homeostasis, and control of other neurohumoral systems, but also leads to excessive production of reactive oxygen species and to hypertrophy, proliferation, migration, and apoptosis of vascular cells. Sodium 119-125 angiotensinogen Homo sapiens 36-50 17057415-6 2006 However, a subgroup of 6 volunteers - showing an increase in sodium excretion after ACE-I - also demonstrated lower AII levels at 13:00 h, a higher cumulative urine flow, and a higher urinary NTproBNP/creatinine excretion in comparison with control (all: p < 0.05). Sodium 61-67 angiotensinogen Homo sapiens 116-119 16142301-8 2005 Interestingly, in this part of the nephron, the effects of aldosterone and angiotensin II are not sodium dependent, whereas in the cortical collecting duct, both aldosterone and angiotensin II, by contrast, affect H+ secretion by sodium-dependent mechanisms. Sodium 230-236 angiotensinogen Homo sapiens 178-192 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 angiotensinogen Homo sapiens 11-25 15669052-2 2005 A-II functions by binding its type 1 (AT1) receptors to cause vasoconstriction and retention of sodium and fluid. Sodium 96-102 angiotensinogen Homo sapiens 0-4 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 angiotensinogen Homo sapiens 133-147 16202699-4 2005 At some point, angiotensin II activates additional mechanisms responsible for sustained increased blood pressure including sodium retention, endothelial dysfunction, and vasoconstriction related to production of reactive oxygen species. Sodium 123-129 angiotensinogen Homo sapiens 15-29 12856080-6 2003 RESULTS: During low sodium, DD-homozygotes showed higher blood pressure sensitivity to angiotensin I ( DD 21+/-5% vs II 15+/-5%, p<0.01). Sodium 20-26 angiotensinogen Homo sapiens 87-100 15252776-4 2004 NO antagonizes the effects of Ang II on vascular tone, cell growth, and renal sodium excretion, and also down-regulates the synthesis of angiotensin-converting enzyme (ACE) and Ang II type 1 receptors. Sodium 78-84 angiotensinogen Homo sapiens 30-36 15160833-6 2004 Chronic exposure to excess angiotensin II produces eccentric ventricular hypertrophy, vasoconstriction, and sodium retention. Sodium 108-114 angiotensinogen Homo sapiens 27-41 15055256-0 2004 High sodium intake strengthens the association between angiotensinogen T174M polymorphism and blood pressure levels among lean men and women: a community-based study. Sodium 5-11 angiotensinogen Homo sapiens 55-70 14675055-0 2004 Angiotensin II receptor blockade prevents acute renal sodium retention induced by low levels of orthostatic stress. Sodium 54-60 angiotensinogen Homo sapiens 0-14 14581294-7 2003 The inverse correlation between angiotensin II and sodium excretion during stress approached significance (r=-0.17; P<0.06). Sodium 51-57 angiotensinogen Homo sapiens 32-46 14597645-7 2003 Angiotensin II infusion reduced renal blood flow, glomerular filtration, sodium excretion, and NO levels in a dose-dependent manner. Sodium 73-79 angiotensinogen Homo sapiens 0-14 15500134-2 2004 All classic physiological effects of AII, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Sodium 105-111 angiotensinogen Homo sapiens 37-40 15272911-7 2004 MEASUREMENTS: Basal and angiotensin II stimulated plasma and 24-h urinary steroid excretion during low (60 mmol/day) and high (160 mmol/day) sodium intake and plasma steroids after ACTH stimulation were measured. Sodium 141-147 angiotensinogen Homo sapiens 24-38 12746271-2 2003 Indeed, some of the properties of the physiologically active component of the RAS, angiotensin II, include vasoconstriction, regulation of renal sodium and water absorption, and increasing thirst. Sodium 145-151 angiotensinogen Homo sapiens 83-97 12801964-8 2003 There was a significant reduction in ANG II and PRA (p<0.05 for each) and the change in ammonia excretion correlated directly with the change in urinary sodium excretion (p<0.007), ANG II (p<0.002), and PRA (p<0.01). Sodium 156-162 angiotensinogen Homo sapiens 187-193 12924618-4 2003 The angiotensinogen gene (AGT) is a thrifty gene which increases the risk for common disease with growth of civilization via sodium and body fluid retention. Sodium 125-131 angiotensinogen Homo sapiens 4-19 12924618-4 2003 The angiotensinogen gene (AGT) is a thrifty gene which increases the risk for common disease with growth of civilization via sodium and body fluid retention. Sodium 125-131 angiotensinogen Homo sapiens 26-29 12737373-2 2003 In pre-ascites, the renal sodium retaining tendency leads to "overfilling" of total blood volume, with increased glomerular filtration rates (GFR), overcoming the renal sodium retaining tendency possibly due to renal accumulation of angiotensin II. Sodium 26-32 angiotensinogen Homo sapiens 233-247 12654713-5 2003 In combination with other genetic or environmental factors (such as dietary sodium intake), we suggest that this might be responsible for the long-term development of a resetting of the aldosterone response to angiotensin II, giving rise to the phenotype of hypertension with a raised ratio. Sodium 76-82 angiotensinogen Homo sapiens 210-224 12676175-6 2003 Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. Sodium 260-266 angiotensinogen Homo sapiens 53-68 12676175-6 2003 Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. Sodium 300-306 angiotensinogen Homo sapiens 53-68 12887132-1 2003 Angiotensin II plays important roles in renal vasoconstriction, sodium reabsorption in proximal tubules, and cell proliferation. Sodium 64-70 angiotensinogen Homo sapiens 0-14 12642013-1 2003 Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute to progressive hypertension and lead to renal and vascular injury. Sodium 88-94 angiotensinogen Homo sapiens 25-39 12642013-1 2003 Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute to progressive hypertension and lead to renal and vascular injury. Sodium 88-94 angiotensinogen Homo sapiens 41-47 12642013-6 2003 The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced distal Ang II formation and sodium reabsorption. Sodium 130-136 angiotensinogen Homo sapiens 22-25 12642013-6 2003 The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced distal Ang II formation and sodium reabsorption. Sodium 130-136 angiotensinogen Homo sapiens 49-52 12642013-7 2003 The augmentation of intrarenal Ang II provides the basis for sustained actions on renal function, sodium excretion, and maintenance of hypertension. Sodium 98-104 angiotensinogen Homo sapiens 31-37 12642017-2 2003 Angiotensin II (Ang II) has stimulatory effects on sodium transport in multiple nephron segments via binding to plasma membrane AT(1) receptors. Sodium 51-57 angiotensinogen Homo sapiens 0-14 12642017-2 2003 Angiotensin II (Ang II) has stimulatory effects on sodium transport in multiple nephron segments via binding to plasma membrane AT(1) receptors. Sodium 51-57 angiotensinogen Homo sapiens 16-22 12642017-4 2003 The stimulatory effect of Ang II on proximal sodium transport is enhanced by renal nerves, and is associated with internalization of apical and basolateral receptors. Sodium 45-51 angiotensinogen Homo sapiens 26-32 14713115-13 2003 Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter, e.g. angiotensin II. Sodium 37-43 angiotensinogen Homo sapiens 113-127 12573139-1 2002 Angiotensin II has been shown to participate in both physiological processes, such as sodium and water homeostasis and vascular contraction, and pathophysiological processes, including atherosclerosis and hypertension. Sodium 86-92 angiotensinogen Homo sapiens 0-14 12527745-12 2003 The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Sodium 32-38 angiotensinogen Homo sapiens 70-75 11471048-3 2001 The effect of Ang II and Ang-(1-7) on renal sodium excretion has been associated, at least in part, with modulation of proximal tubule sodium reabsorption. Sodium 44-50 angiotensinogen Homo sapiens 14-20 11912262-0 2002 Enhanced responses of blood pressure, renal function, and aldosterone to angiotensin I in the DD genotype are blunted by low sodium intake. Sodium 125-131 angiotensinogen Homo sapiens 73-86 11881132-3 2001 Angiotensin II (Ang II) increases sodium reabsorption and hence oxygen consumption at any given bloodflow rate; therefore, it may affect the balance of renal oxygen supply vs. demand and hence Epo production. Sodium 34-40 angiotensinogen Homo sapiens 0-14 11881132-3 2001 Angiotensin II (Ang II) increases sodium reabsorption and hence oxygen consumption at any given bloodflow rate; therefore, it may affect the balance of renal oxygen supply vs. demand and hence Epo production. Sodium 34-40 angiotensinogen Homo sapiens 16-22 11912262-6 2002 With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes +/- 95% confidence intervals), with mean MAP increases of 22 +/- 2% (DD genotype), 13 +/- 5% (ID genotype), and 12 +/- 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 +/- 19.7% (DD genotype), 73.0 +/- 16.3% (ID genotype), and 63.2 +/- 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 +/- 189% (DD genotype), 343 +/- 71% (ID genotype), and 254 +/- 99% (II genotype) (P < 0.05). Sodium 13-19 angiotensinogen Homo sapiens 107-111 11912262-9 2002 In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. Sodium 22-28 angiotensinogen Homo sapiens 54-58 11799146-1 2002 Angiotensin II (Ang II) regulates water and sodium transport in renal tubules and gastrointestinal tract. Sodium 44-50 angiotensinogen Homo sapiens 0-14 11799146-1 2002 Angiotensin II (Ang II) regulates water and sodium transport in renal tubules and gastrointestinal tract. Sodium 44-50 angiotensinogen Homo sapiens 16-22 12036384-9 2002 The AT(1) receptor is responsible for the majority of the effects of angiotensin II: vasoconstriction, sodium re-absorption, cell proliferation, extracellular matrix formation, inflammatory response and oxidative stress. Sodium 103-109 angiotensinogen Homo sapiens 69-83 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 angiotensinogen Homo sapiens 16-30 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 angiotensinogen Homo sapiens 32-38 12036388-4 2002 The AT(1 )receptor mediates all of the known actions of Ang II in the cardiovascular system, such as vasoconstriction, increasing cardiac contractility and renal tubular sodium reabsorption, as well as vascular and cardiac hypertrophy. Sodium 170-176 angiotensinogen Homo sapiens 56-62 11828179-4 2001 The role of angiotensin II in controlling sodium balance, in both renal insufficiency states and congestive heart failure, is clearly recognized. Sodium 42-48 angiotensinogen Homo sapiens 12-26 11471048-3 2001 The effect of Ang II and Ang-(1-7) on renal sodium excretion has been associated, at least in part, with modulation of proximal tubule sodium reabsorption. Sodium 135-141 angiotensinogen Homo sapiens 14-20 11333009-1 2001 Among the many roles that angiotensin II plays in the kidney, one of the most important is the direct and indirect regulation of sodium excretion. Sodium 129-135 angiotensinogen Homo sapiens 26-40 11479173-12 2001 Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter (eg, angiotensin II). Sodium 37-43 angiotensinogen Homo sapiens 112-126 11244019-7 2001 This abnormality in sodium handling during activation of the sympathetic nervous system appears to be mediated by angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 114-128 11230340-1 2001 Angiotensin (Ang) II is considered a regulatory hormone stimulating vascular smooth muscle cell constriction, aldosterone release from the adrenal gland, and sodium reabsorption in the renal tubule. Sodium 158-164 angiotensinogen Homo sapiens 0-20 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 angiotensinogen Homo sapiens 43-57 11403985-2 2001 ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and pressor responses. Sodium 48-54 angiotensinogen Homo sapiens 0-6 11403985-4 2001 Previous injection of a nonselective alpha-adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and pressor responses induced by ANG II injected into the MSA. Sodium 145-151 angiotensinogen Homo sapiens 208-214 11333009-3 2001 High levels of angiotensin II subtype 1 receptors have been detected on the luminal side of the tubular cells in the proximal convoluted tubule, and these have been implicated in the regulation of sodium excretion. Sodium 197-203 angiotensinogen Homo sapiens 15-29 11333009-5 2001 It is, therefore, reasonable to assume that blockade of these receptors, using non-peptide angiotensin II receptor antagonists, will bring about an increase in renal excretion of sodium. Sodium 179-185 angiotensinogen Homo sapiens 91-105 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 angiotensinogen Homo sapiens 43-57 21331734-2 2001 One major function is the reabsorption of sodium and other electrolytes which is caused, in part, by angiotensin II (Ang II), a peptide that is made up of eight amino acids. Sodium 42-48 angiotensinogen Homo sapiens 101-115 21331734-2 2001 One major function is the reabsorption of sodium and other electrolytes which is caused, in part, by angiotensin II (Ang II), a peptide that is made up of eight amino acids. Sodium 42-48 angiotensinogen Homo sapiens 117-123 11136161-8 2001 Although glucocorticoids themselves produce no increase in sodium reabsorption in this segment, angiotensin II-stimulated sodium transport is significantly greater in proximal tubular cells pretreated with glucocorticoids. Sodium 122-128 angiotensinogen Homo sapiens 96-110 11517684-0 2001 [Effects of anti-atherosclerotic low-sodium diet on dynamics of natural antibodies to angiotensin II, bradykinin and vasopressin in blood of patients with hypertension and obesity]. Sodium 37-43 angiotensinogen Homo sapiens 86-100 11081765-2 2000 A diminished capacity to excrete sodium secondary to increased proximal tubular re-absorption and loss of the renal functional reserve are the two most relevant initial alterations of renal function in which angiotensin II has been proven to act directly. Sodium 33-39 angiotensinogen Homo sapiens 208-222 10981548-1 2000 Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. Sodium 25-31 angiotensinogen Homo sapiens 0-14 10981548-1 2000 Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. Sodium 118-124 angiotensinogen Homo sapiens 0-14 10981548-6 2000 Sodium excretion in response to 3.0 ng/kg/min angiotensin II was diminished in both groups (P < .01). Sodium 0-6 angiotensinogen Homo sapiens 46-60 10981548-8 2000 We conclude that increased sodium retention in response to angiotensin II exists in subjects with essential hypertension, which is unrelated to changes in glomerular filtration rate and aldosterone concentration. Sodium 27-33 angiotensinogen Homo sapiens 59-73 10981548-9 2000 Our data suggest a hyperresponsiveness to angiotensin II in essential hypertension that could lead to increased sodium retention. Sodium 112-118 angiotensinogen Homo sapiens 42-56 10994750-1 2000 OBJECTIVE: To examine the interaction of sodium intake with genetic variations of the angiotensinogen gene and hypertension. Sodium 41-47 angiotensinogen Homo sapiens 86-101 10994750-12 2000 CONCLUSION: Angiotensinogen genotype may affect the development of early-onset hypertension among Japanese, particularly in those who have a high sodium intake. Sodium 146-152 angiotensinogen Homo sapiens 12-27 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 135-141 angiotensinogen Homo sapiens 30-44 10988274-0 2000 Angiotensin II sensitivity is associated with the angiotensin II type 1 receptor A(1166)C polymorphism in essential hypertensives on a high sodium diet. Sodium 140-146 angiotensinogen Homo sapiens 0-14 10988274-0 2000 Angiotensin II sensitivity is associated with the angiotensin II type 1 receptor A(1166)C polymorphism in essential hypertensives on a high sodium diet. Sodium 140-146 angiotensinogen Homo sapiens 50-64 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 135-141 angiotensinogen Homo sapiens 46-52 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 30-44 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 46-52 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 30-44 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 46-52 11022893-4 2000 An inability to suppress Ang II formation in response to increases in sodium intake can lead to salt-sensitive hypertension. Sodium 70-76 angiotensinogen Homo sapiens 25-31 11022893-5 2000 Excess formation of Ang II, such as in renovascular hypertension, causes the pressure natriuresis relationship to be shifted to higher arterial pressures so that higher arterial pressures are necessary to maintain sodium balance. Sodium 214-220 angiotensinogen Homo sapiens 20-26 11022893-7 2000 Because Ang II does not decrease glomerular filtration in most circumstances, the sodium retaining actions of Ang II are usually caused by increased tubular reabsorption. Sodium 82-88 angiotensinogen Homo sapiens 110-116 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 angiotensinogen Homo sapiens 15-21 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 angiotensinogen Homo sapiens 100-113 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 angiotensinogen Homo sapiens 178-184 10691781-7 2000 In the gastrointestinal tract, physiological quantities of ANG II stimulate the AT2 receptor releasing NO and cGMP leading to increased sodium and water absorption. Sodium 136-142 angiotensinogen Homo sapiens 59-65 10619573-4 1999 Angiotensin II also alters renal sodium and water absorption through its ability to stimulate the zona glomerulosa cells of the adrenal cortex to synthesize and secrete aldosterone. Sodium 33-39 angiotensinogen Homo sapiens 0-14 10618583-2 2000 Recent treatment strategies have focused on attenuating the effects of angiotensin (Ang) II, which include vasoconstriction, sodium retention, sympathetic activation, and cell growth. Sodium 125-131 angiotensinogen Homo sapiens 71-91 10539810-1 1999 BACKGROUND: High angiotensin II levels in relation to the corresponding urinary sodium excretion have been found to modulate left ventricular (LV) structure in middle-aged hypertensive patients. Sodium 80-86 angiotensinogen Homo sapiens 17-31 10619595-2 1999 Because Ang II affects blood pressure control, sodium and water homeostasis, and cardiovascular function and structure, a great deal of research effort has been directed toward blocking the RAS. Sodium 47-53 angiotensinogen Homo sapiens 8-14 10601129-2 1999 We show that polarized epithelium of the proximal tubule synthesizes and secretes angiotensinogen at its apical side and that the protein can be detected in urine as a function of dietary sodium. Sodium 188-194 angiotensinogen Homo sapiens 82-97 10594793-11 1999 CONCLUSIONS: Taken together, these results suggest that there is a relationship between the AGT1R A1166-->C polymorphism and the humoral and renal hemodynamic responses to AGT1R blockade and to Ang II infusion in the sodium-replete state, and that the C allele is associated with enhanced intrarenal and peripheral Ang II activity. Sodium 220-226 angiotensinogen Homo sapiens 197-203 10594793-11 1999 CONCLUSIONS: Taken together, these results suggest that there is a relationship between the AGT1R A1166-->C polymorphism and the humoral and renal hemodynamic responses to AGT1R blockade and to Ang II infusion in the sodium-replete state, and that the C allele is associated with enhanced intrarenal and peripheral Ang II activity. Sodium 220-226 angiotensinogen Homo sapiens 318-324 10539810-8 1999 The increase of sodium excretion at high salt intake was related to a physiologically expected decrease of angiotensin II and aldosterone levels in normotensive (r = -0.36, P <.01 and r = -0.32; P =.016, respectively) but not in hypertensive patients. Sodium 16-22 angiotensinogen Homo sapiens 107-121 10516741-10 1999 However, hypertensives have a delay in resetting the adrenal responsiveness to angiotensin II suggesting that they have altered sodium perception during rapid changes in salt balance. Sodium 128-134 angiotensinogen Homo sapiens 79-93 10437737-2 1999 Angiotensin II is the principal effector hormone in the RAS, causing vasoconstriction and increased sodium and water retention, leading to increased blood pressure. Sodium 100-106 angiotensinogen Homo sapiens 0-14 10516741-1 1999 We investigated sodium and volume-dependent mechanisms in the modulation of adrenal and renal vascular responsiveness to angiotensin II in hypertensive (n = 9) and normal subjects (n = 5) who demonstrated normal responses during steady-state salt balance (intact modulation). Sodium 16-22 angiotensinogen Homo sapiens 121-135 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 66-72 angiotensinogen Homo sapiens 54-60 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 angiotensinogen Homo sapiens 54-60 10361442-2 1999 In addition, AngII enhances tubular reabsorption of sodium in proximal tubules directly and indirectly as a consequence of glomerulotubular balance. Sodium 52-58 angiotensinogen Homo sapiens 13-18 10342783-0 1999 Enhanced blood pressure response to mild sodium reduction in subjects with the 235T variant of the angiotensinogen gene. Sodium 41-47 angiotensinogen Homo sapiens 99-114 10342783-8 1999 The angiotensinogen gene accounts for some of the interindividual variation of the blood pressure response to sodium reduction. Sodium 110-116 angiotensinogen Homo sapiens 4-19 10361429-3 1999 Angiotensin II in the brain increases water and sodium intake, raises blood pressure, attenuates baro-reflex function, and increases vasopressin secretion. Sodium 48-54 angiotensinogen Homo sapiens 0-14 10342788-2 1999 We have recently shown that this endogenously produced and luminally secreted angiotensin II regulates proximal tubule volume reabsorption, which is a reflection of sodium transport within this segment. Sodium 165-171 angiotensinogen Homo sapiens 78-92 10201880-7 1999 However, when AngII levels are inappropriately elevated, this necessitates increased arterial pressure to maintain sodium and water balance. Sodium 115-121 angiotensinogen Homo sapiens 14-19 10981059-6 1999 This action of angiotensin II occurs when the renin-angiotensin system is activated, as in sodium depletion. Sodium 91-97 angiotensinogen Homo sapiens 15-29 10372513-0 1999 Effects of the alpha antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by angiotensin II injection into the subfornical organ. Sodium 102-108 angiotensinogen Homo sapiens 127-141 10372513-5 1999 Previous administration of clonidine (an alpha2-adrenergic agonist) or noradrenaline into the LH increased, whereas pretreatment with phenylephrine decreased the sodium intake induced by injection of ANG II into the SFO. Sodium 162-168 angiotensinogen Homo sapiens 200-206 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 angiotensinogen Homo sapiens 167-181 10067792-11 1999 CONCLUSIONS: In sodium-depleted subjects, endogenous angiotensin II appears to play a role in the regulation of forearm vascular tone, in contrast to sodium-replete conditions. Sodium 16-22 angiotensinogen Homo sapiens 53-67 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 angiotensinogen Homo sapiens 183-189 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 angiotensinogen Homo sapiens 167-181 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 angiotensinogen Homo sapiens 183-189 9893137-13 1999 CONCLUSIONS: The renal microcirculation in sodium-replete women may respond differently to Ang II than that of men, with the female sex predicting a lesser augmentation of FF and possibly a blunted increase in intraglomerular pressure. Sodium 43-49 angiotensinogen Homo sapiens 91-97 9892162-5 1999 Although the mechanisms responsible for the regulation of intratubular AngII concentrations remain to be determined, micropuncture studies have provided direct evidence that activation of intraluminal AT1 receptors by AngII exerts a substantial stimulatory influence on sodium and bicarbonate transport by both proximal and distal tubules. Sodium 270-276 angiotensinogen Homo sapiens 218-223 10076924-5 1999 These findings suggest that inhibition of angiotensin II action by candesartan can improve insulin sensitivity and inhibit the sodium-retaining action associated with hyperinsulinaemia in essential hypertension. Sodium 127-133 angiotensinogen Homo sapiens 42-56 10207252-8 1999 Second, activation of the tubuloglomerular feedback system enhances intrarenal angiotensin II release, which augments proximal sodium absorption. Sodium 127-133 angiotensinogen Homo sapiens 79-93 9860786-2 1998 Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Sodium 78-84 angiotensinogen Homo sapiens 130-144 9860786-2 1998 Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Sodium 78-84 angiotensinogen Homo sapiens 146-149 9855025-2 1998 Because angiotensin II affects blood pressure control, sodium and water homeostasis, and cardiovascular function and structure, a great deal of research effort has been directed toward blocking the renin-angiotensin system. Sodium 55-61 angiotensinogen Homo sapiens 8-22 9740601-10 1998 We conclude that the angiotensinogen genotype may affect blood pressure response to sodium or weight reduction and the development of hypertension. Sodium 84-90 angiotensinogen Homo sapiens 21-36 9703338-3 1998 Moreover, under high-sodium conditions, angiotensin II infusion (3 ng x kg(-1) x min(-1)) caused a greater increase in mean BP (14 +/- 2 vs. 7.4 +/- 1 mmHg; P < 0.05) and a smaller reduction in renal plasma flow (-122 +/- 29 vs. -274 +/- 41 ml x min(-1) x 1.73 m2; P < 0.05) in microalbuminuric than in normoalbuminuric IDDM patients. Sodium 21-27 angiotensinogen Homo sapiens 40-54 9703338-4 1998 Under low sodium conditions, aldosterone increments after angiotensin II infusion were lower (P < 0.05) in microalbuminuric than in normoalbuminuric IDDM patients. Sodium 10-16 angiotensinogen Homo sapiens 58-72 8976805-13 1996 In the whole population of patients with non-insulin-dependent diabetes mellitus, the increase in intracellular pH after exposure to angiotensin II was positively correlated with intracellular free calcium increase (r = 0.53; P < 0.05), suggesting a possible role of intracellular free calcium levels in the activation of the sodium-hydrogen antiport. Sodium 329-335 angiotensinogen Homo sapiens 133-147 9674690-1 1998 Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. Sodium 90-96 angiotensinogen Homo sapiens 0-20 9674690-17 1998 But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Sodium 59-65 angiotensinogen Homo sapiens 121-127 9674690-18 1998 Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetit Sodium 279-285 angiotensinogen Homo sapiens 8-14 9589654-7 1998 Dietary sodium restriction may result in a decrease in peripheral insulin sensitivity in normotensive patients with NIDDM, possibly via an elevation in prevailing angiotensin II concentrations. Sodium 8-14 angiotensinogen Homo sapiens 163-177 9930375-4 1998 ANG-II regulates blood pressure by controlling sodium reabsorption in the proximal tubule, altering the glomerular filtration rate and renal blood flow, and by modifying the production and release of aldosterone in the adrenal gland. Sodium 47-53 angiotensinogen Homo sapiens 0-6 9861615-6 1998 Circulating hormones like angiotensin II and adrenocorticotropin hormone, which are released in response to sodium deficiency and adrenalectomy, could regulate the activity of Na+ channels through G-protein linked second-messenger systems. Sodium 108-114 angiotensinogen Homo sapiens 26-40 9463638-8 1997 Sodium depletion elevated plasma renin activity and angiotensin II concentrations (p < or = 0.002) after which acute local administration of losartan increased forearm blood flow in a dose dependent manner (maximum of 69 +/- 17%; p < 0.001). Sodium 0-6 angiotensinogen Homo sapiens 52-66 9170000-1 1997 BACKGROUND: Results from previous studies suggested that a blunted response of renal plasma flow (RPF) to angiotensin II infusion during a high-sodium diet (a phenotype associated with nonmodulation) is an intermediate phenotype for essential hypertension. Sodium 144-150 angiotensinogen Homo sapiens 106-120 9043811-12 1997 Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension. Sodium 140-146 angiotensinogen Homo sapiens 76-81 9543596-1 1998 BACKGROUND: In a previous study we found that high angiotensin II levels in relation to the corresponding urinary sodium excretion aggravate left ventricular hypertrophy in hypertensive patients. Sodium 114-120 angiotensinogen Homo sapiens 51-65 9543596-9 1998 Subgroup analysis revealed that the increase in sodium excretion at high salt intake was related to the decrease in angiotensin II levels in normotensive (r = -0.43, p < 0.05), but not in hypertensive subjects (r = 0.16, n.s.). Sodium 48-54 angiotensinogen Homo sapiens 116-130 9463638-0 1997 Endogenous angiotensin II contributes to basal peripheral vascular tone in sodium deplete but not sodium replete man. Sodium 75-81 angiotensinogen Homo sapiens 11-25 9430825-12 1997 These data suggest a physiologic role of sodium balance (possibly mediated via endogenous AII) in the control of thirst in normal humans. Sodium 41-47 angiotensinogen Homo sapiens 90-93 9369271-6 1997 In addition, we found that in the diabetic patients on a high sodium diet, the renal blood flow response to exogenous angiotensin II was not bimodally distributed, as is the case in essential hypertension, in which a subgroup of the patients are characterized by sodium sensitivity of the blood pressure and an abnormal renal blood flow response to exogenous angiotensin II ("nonmodulator phenotype"). Sodium 62-68 angiotensinogen Homo sapiens 118-132 9369271-6 1997 In addition, we found that in the diabetic patients on a high sodium diet, the renal blood flow response to exogenous angiotensin II was not bimodally distributed, as is the case in essential hypertension, in which a subgroup of the patients are characterized by sodium sensitivity of the blood pressure and an abnormal renal blood flow response to exogenous angiotensin II ("nonmodulator phenotype"). Sodium 263-269 angiotensinogen Homo sapiens 118-132 9247766-0 1997 Pharmacological demonstration of the additive effects of angiotensin-converting enzyme inhibition and angiotensin II antagonism in sodium depleted healthy subjects. Sodium 131-137 angiotensinogen Homo sapiens 102-116 9170001-4 1997 RESULTS: There was some evidence that measures of the renal plasma flow and of its response to angiotensin II infusion during the high-sodium diet were statistically significant predictors of measures of blood pressure in women; there was less evidence for this for blood pressures in men. Sodium 135-141 angiotensinogen Homo sapiens 95-109 9468457-15 1997 This was observed in patients as well as in healthy subjects, but the effects of Ang II on renal haemodynamics and sodium handling were more pronounced in diabetic patients. Sodium 115-121 angiotensinogen Homo sapiens 81-87 9468457-17 1997 In contrast, the effects of Ang II on renal perfusion and sodium handling are more pronounced in patients with NIDDM than they are in healthy subjects. Sodium 58-64 angiotensinogen Homo sapiens 28-34 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 angiotensinogen Homo sapiens 57-72 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 angiotensinogen Homo sapiens 156-170 8934356-2 1996 BACKGROUND: Non-modulating hypertensives are a subset of sodium-sensitive hypertensives characterized by a failure to modulate renal, vascular and adrenal glomerulosa responsivenesses to angiotensin II appropriately. Sodium 57-63 angiotensinogen Homo sapiens 187-201 8945678-5 1996 In contrast, a nonpressor dose of angiotensin II (3 ng/min) reduced basal sodium excretion and the natriuretic responses to exogenous hANP 99-126 in the presence or absence of BMS-182657. Sodium 74-80 angiotensinogen Homo sapiens 34-48 8822984-7 1996 Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion. Sodium 56-62 angiotensinogen Homo sapiens 19-25 8873664-5 1996 In a normal sodium diet, angiotensin I and II aorta-coronary sinus gradients were tendentially negative (-1.8 +/- 2.5 and -0.9 +/- 1.7 pg/mL, respectively), and the amounts of angiotensin I and II added by cardiac tissues were 6.5 +/- 3.1 and 2.7 +/- 1.3 pg/mL, respectively. Sodium 12-18 angiotensinogen Homo sapiens 25-45 9387775-2 1996 The effect of microinjection of A II into the AP on renal sodium excretion was studied in the present investigation. Sodium 58-64 angiotensinogen Homo sapiens 32-36 9387775-6 1996 These results strongly suggest that the A II induced changes of renal hemodynamics and urine sodium excretion are mediated through AP. Sodium 93-99 angiotensinogen Homo sapiens 40-44 8873664-6 1996 The low sodium diet caused a significant increase in both plasma renin activity (PRA) and angiotensin I concentration in aortic but not in coronary sinus blood, resulting in a more negative aorta-coronary sinus gradient (-9.7 +/- 3.1 pg/mL, P < .01). Sodium 8-14 angiotensinogen Homo sapiens 90-103 8822984-0 1996 Angiotensin II related to sodium excretion modulates left ventricular structure in human essential hypertension. Sodium 26-32 angiotensinogen Homo sapiens 0-14 8822984-2 1996 We conducted a study to investigate the interaction of sodium excretion with Ang II and its potential impact on myocardial hypertrophy. Sodium 55-61 angiotensinogen Homo sapiens 77-83 8822984-7 1996 Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion. Sodium 369-375 angiotensinogen Homo sapiens 19-25 8864421-14 1996 Net sodium excretion during the combined infusion with ANG II and ANP seems to reflect the sum of the opposing influences of each peptide. Sodium 4-10 angiotensinogen Homo sapiens 55-61 21143283-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 angiotensinogen Homo sapiens 48-62 21143283-9 1996 Angiotensin II affects transepithelial sodium transport by modulation of Na(+) /H(+) exchange at the luminal membrane and Na(+)/HCO(3) cotransport, Na(+)/K(+)-ATPase activity and K(+) conductance at the basolateral membrane. Sodium 39-45 angiotensinogen Homo sapiens 0-14 21143284-9 1996 The expression of the AT(1) receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT(1) receptor mRNA levels and binding and increase aldosterone secretion. Sodium 144-150 angiotensinogen Homo sapiens 133-138 8864421-4 1996 ANG II alone caused a decrease in glomerular filtration rate (GFR), renal plasma flow, urinary absolute and fractional excretion of sodium, both proximal and distal fractional tubular sodium reabsorption, and urinary flow. Sodium 132-138 angiotensinogen Homo sapiens 0-6 8864421-4 1996 ANG II alone caused a decrease in glomerular filtration rate (GFR), renal plasma flow, urinary absolute and fractional excretion of sodium, both proximal and distal fractional tubular sodium reabsorption, and urinary flow. Sodium 184-190 angiotensinogen Homo sapiens 0-6 8864421-8 1996 ANG II + ANP: during a background ANG II infusion, ANP still increased fractional excretion of sodium. Sodium 95-101 angiotensinogen Homo sapiens 0-6 7721403-0 1995 Angiotensin II and sympathetic activity in sodium-restricted essential hypertension. Sodium 43-49 angiotensinogen Homo sapiens 0-14 7641363-0 1995 Additive effects of combined angiotensin-converting enzyme inhibition and angiotensin II antagonism on blood pressure and renin release in sodium-depleted normotensives. Sodium 139-145 angiotensinogen Homo sapiens 74-88 8660367-5 1996 Both pH recovery after angiotensin II and alkalinization after aldosterone were blocked in sodium-free medium. Sodium 91-97 angiotensinogen Homo sapiens 23-37 8732994-4 1996 However, the increase in AII is sufficient for a slight reduction in renal blood flow and a slight increase in exchangeable sodium and blood pressure; in susceptible women, blood pressure may rise considerably. Sodium 124-130 angiotensinogen Homo sapiens 25-28 8993849-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 angiotensinogen Homo sapiens 48-62 8993849-9 1996 Angiotensin II affects transepithelial sodium transport by modulation of Na+/H+ exchange at the luminal membrane and Na+/HCO3 cotransport, Na+/K(+)-ATPase activity and K+ conductance at the basolateral membrane. Sodium 39-45 angiotensinogen Homo sapiens 0-14 8993850-9 1996 The expression of the AT1 receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT1 receptor mRNA levels and binding and increase aldosterone secretion. Sodium 142-148 angiotensinogen Homo sapiens 131-136 8649652-11 1996 Angiotensin II elicited a further increase in distal fractional tubular sodium reabsorption in both groups (P < 0.05). Sodium 72-78 angiotensinogen Homo sapiens 0-14 8649652-13 1996 Angiotensin II caused further sodium retention, probably due to an effect on renal haemodynamics. Sodium 30-36 angiotensinogen Homo sapiens 0-14 8583471-11 1995 Accordingly, we found that relatively too high levels of angiotensin II in relation to urinary sodium excretion were associated with left ventricular hypertrophy in these individuals on high salt intake. Sodium 95-101 angiotensinogen Homo sapiens 57-71 7611241-4 1995 Both angiotensin II antagonists induced a significant increase in urinary sodium excretion. Sodium 74-80 angiotensinogen Homo sapiens 5-19 7833591-7 1994 Furthermore, aging is associated with a reduced adrenal responsiveness to angiotensin II, contributing to lower production of aldosterone and alterations of sodium homeostasis. Sodium 157-163 angiotensinogen Homo sapiens 74-88 7854155-9 1995 In contrast, infusion of equipressor doses of Ang II decreased urinary sodium excretion and did not significantly alter the excretion of ET. Sodium 71-77 angiotensinogen Homo sapiens 46-52 7884582-4 1994 Like ACE inhibitors, the angiotensin II inhibitors TCV 116 and losartan cause a marked impairment in the renal adaptation to dietary sodium restriction, suggesting that blockade of the renin-angiotensin system is primarily involved in this process. Sodium 133-139 angiotensinogen Homo sapiens 25-39 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 angiotensinogen Homo sapiens 93-107 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 angiotensinogen Homo sapiens 194-208 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 angiotensinogen Homo sapiens 93-107 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 angiotensinogen Homo sapiens 93-107 8304488-0 1994 Angiotensin II suppression is a major factor permitting excretion of an acute sodium load in humans. Sodium 78-84 angiotensinogen Homo sapiens 0-14 7531080-3 1994 A high sodium intake can overcome the effect of the lack of angiotensin II. Sodium 7-13 angiotensinogen Homo sapiens 60-74 7811436-5 1994 This patient consistently demonstrated an abnormally low plasma aldosterone response to AII (3 ng/kg/min) on a low salt (10 mEq sodium) diet while both normotensive and hypertensive. Sodium 128-134 angiotensinogen Homo sapiens 88-91 8018457-2 1994 As compared with placebo, angiotensin II infusion alone caused significant reductions in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.001 vs placebo) but had no effect on glomerular filtration rate. Sodium 106-112 angiotensinogen Homo sapiens 26-40 8018457-2 1994 As compared with placebo, angiotensin II infusion alone caused significant reductions in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.001 vs placebo) but had no effect on glomerular filtration rate. Sodium 135-141 angiotensinogen Homo sapiens 26-40 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 163-169 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 163-169 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 192-198 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 192-198 angiotensinogen Homo sapiens 93-107 8242257-12 1993 When 6 micrograms kg-1 h-1 of angiotensin II was infused directly into the fetus RBF fell from 69 +/- 10.1 ml min-1 to 31 +/- 13.9 ml min-1, GFR rose (P < 0.05) and urine flow (P < 0.01) and sodium excretion increased in all fetuses. Sodium 197-203 angiotensinogen Homo sapiens 30-44 7816287-4 1994 Absolute proximal reabsorption of sodium was increased at baseline in the diabetic group, and fell during ANGII. Sodium 34-40 angiotensinogen Homo sapiens 106-111 7816287-9 1994 Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms. Sodium 188-194 angiotensinogen Homo sapiens 64-78 7816287-9 1994 Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms. Sodium 188-194 angiotensinogen Homo sapiens 120-134 8403783-17 1993 Pressor doses of angiotensin II also have a significant effect on the distal tubule in promoting sodium reabsorption. Sodium 97-103 angiotensinogen Homo sapiens 17-31 8218608-2 1993 Short-term dietary sodium intake is a known modulator of blood pressure response to infused angiotensin II (A II) in normal subjects. Sodium 19-25 angiotensinogen Homo sapiens 92-106 8218608-2 1993 Short-term dietary sodium intake is a known modulator of blood pressure response to infused angiotensin II (A II) in normal subjects. Sodium 19-25 angiotensinogen Homo sapiens 108-112 8218608-7 1993 Our results indicate that it requires long time before decreased A II responsiveness caused by chronic sodium depletion normalizes in AN patients. Sodium 103-109 angiotensinogen Homo sapiens 65-69 8403783-11 1993 In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min-1 kg-1. Sodium 45-51 angiotensinogen Homo sapiens 27-41 8403783-14 1993 The fractional distal reabsorption of sodium, determined by using the lithium clearance technique, showed a rise with all doses of angiotensin II used and reached statistical significance with the top two doses. Sodium 38-44 angiotensinogen Homo sapiens 131-145 8230088-7 1993 Intravascular angiotensin II receptors are implicated in the central release of vasopressin and other hypophyseal hormones, in increasing sympathetic outflow, in the thirst response and, possibly, in cognitive function; in the inotropic and chronotropic effects of angiotensin II on the heart as well as in growth/hypertrophy; in the control of aldosterone release and in the balance between cortisol and aldosterone secretion; and in modulating sodium, chloride and bicarbonate transport within the kidney. Sodium 446-452 angiotensinogen Homo sapiens 14-28 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 angiotensinogen Homo sapiens 71-91 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 angiotensinogen Homo sapiens 9-15 8478039-7 1993 The blood pressure response to Ang II, on the other hand, was greater in salt-sensitive than salt-resistant patients during low but not during high sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 31-37 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 angiotensinogen Homo sapiens 113-127 8478039-11 1993 In fact, we observed increased reactivity to Ang II during low but not during high sodium intake. Sodium 83-89 angiotensinogen Homo sapiens 45-51 8098306-8 1993 Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. Sodium 98-104 angiotensinogen Homo sapiens 228-242 8498970-6 1993 These prostaglandins may attenuate any direct Ang II-induced vasoconstriction, lower systemic vascular resistance and stimulate renal sodium excretion. Sodium 134-140 angiotensinogen Homo sapiens 46-52 1328362-1 1992 OBJECTIVE: The aim was to study the physiological effects of angiotensin II upon the glomerular and tubular handling of sodium. Sodium 120-126 angiotensinogen Homo sapiens 61-75 1336524-1 1992 OBJECTIVE: The present study examines the role of alpha 1-adrenoceptors in determining the renal haemodynamic and sodium excretory responses to a physiological dose of angiotensin II in man. Sodium 114-120 angiotensinogen Homo sapiens 168-182 1336524-8 1992 Angiotensin II alone also increased fractional reabsorption of sodium delivered to the distal nephron, as evaluated by both the CLi method and by estimation of solute-free water clearance. Sodium 63-69 angiotensinogen Homo sapiens 0-14 1336524-10 1992 CONCLUSIONS: These findings suggest that low doses of circulating angiotensin II are able to modulate UNaV by increasing sodium reabsorption in the proximal and, to some extent, the distal nephron segment in man. Sodium 121-127 angiotensinogen Homo sapiens 66-80 7922165-7 1993 Local angiotensin II production can have profound influences on renal function, ie, alter glomerular hemodynamics, reduce sodium excretion, and constrict small arterioles. Sodium 122-128 angiotensinogen Homo sapiens 6-20 1471538-6 1992 In conclusion, increased A II sensitivity caused by chronic sodium deficiency in AN patients normalized over time as the patients recovered. Sodium 60-66 angiotensinogen Homo sapiens 25-29 1328362-6 1992 Angiotensin II caused an extensive and instantaneous fall in both urinary flow and urinary sodium excretion. Sodium 91-97 angiotensinogen Homo sapiens 0-14 1328362-9 1992 However, when the distal reabsorption was related to the delivery of sodium from the proximal tubules, distal fractional reabsorption in fact increased after 30 min angiotensin II infusion. Sodium 69-75 angiotensinogen Homo sapiens 165-179 1328362-14 1992 The antinatriuretic effect of angiotensin II is caused initially by a combination of a decrease in the GFR and an increase in proximal fractional sodium reabsorption, and later by the enhanced distal fractional reabsorption of sodium. Sodium 146-152 angiotensinogen Homo sapiens 30-44 1328362-14 1992 The antinatriuretic effect of angiotensin II is caused initially by a combination of a decrease in the GFR and an increase in proximal fractional sodium reabsorption, and later by the enhanced distal fractional reabsorption of sodium. Sodium 227-233 angiotensinogen Homo sapiens 30-44 1317764-7 1992 The fall in fractional sodium excretion during angiotensin II infusion was reduced after pretreatment with 750 mg of lithium [750 mg of lithium, 2.73 (0.24) to 1.34 (0.08)%; placebo, 2.69 (0.26) to 1.01 (0.11)%; P = 0.02]. Sodium 23-29 angiotensinogen Homo sapiens 47-61 1366263-12 1992 Thus, elevations in circulating aldosterone and angiotensin II, relative to sodium intake, have the potential to not only alter sodium homeostasis and vascular tonicity, but also the structure of cardiovascular tissue. Sodium 128-134 angiotensinogen Homo sapiens 48-62 1535400-2 1992 Theoretically, reversal of the sodium-retaining effect of angiotensin II (Ang II) could be involved. Sodium 31-37 angiotensinogen Homo sapiens 58-72 1535400-2 1992 Theoretically, reversal of the sodium-retaining effect of angiotensin II (Ang II) could be involved. Sodium 31-37 angiotensinogen Homo sapiens 74-80 1535400-11 1992 The fact that felodipine reverses sodium retention on exogenous Ang II may be explained by interference with systemic and renal hemodynamic effects of exogenous Ang II. Sodium 34-40 angiotensinogen Homo sapiens 64-70 1331894-1 1992 The antinatriuretic effect of angiotensin II (Ang II) is generally attributed to a decreased glomerular filtration rate (GFR) and an increased proximal tubular sodium reabsorption. Sodium 160-166 angiotensinogen Homo sapiens 30-44 1580276-1 1992 Angiotensin II plays an important role in the kidney by regulating renal flow, glomerular filtration rate, mesangial cell function, and sodium reabsorption. Sodium 136-142 angiotensinogen Homo sapiens 0-14 1516268-15 1992 It is concluded that intrarenal AII acts to maintain optimal matching of fluid reabsorption and filtered load in response to changes in sodium balance, as well as to promote acidification of the urine during acidosis and perhaps to potentiate tubular growth following renal injury. Sodium 136-142 angiotensinogen Homo sapiens 32-35 1331894-1 1992 The antinatriuretic effect of angiotensin II (Ang II) is generally attributed to a decreased glomerular filtration rate (GFR) and an increased proximal tubular sodium reabsorption. Sodium 160-166 angiotensinogen Homo sapiens 46-52 1331894-9 1992 These data suggest that the antinatriuretic effect of modestly hypertensive dosages of Ang II is not only due to a decrease in GFR and an increase in proximal sodium reabsorption, but also involves a rise in fractional reabsorption in a distal nephron segment. Sodium 159-165 angiotensinogen Homo sapiens 87-93 1741989-5 1991 Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Sodium 69-75 angiotensinogen Homo sapiens 143-157 1937678-6 1991 In normal subjects, the response of the adrenal glomerulosa cell to Ang II varies with the level of sodium intake, with sodium restriction enhancing the response. Sodium 100-106 angiotensinogen Homo sapiens 68-74 1937678-6 1991 In normal subjects, the response of the adrenal glomerulosa cell to Ang II varies with the level of sodium intake, with sodium restriction enhancing the response. Sodium 120-126 angiotensinogen Homo sapiens 68-74 1412446-5 1992 Both Ang II and ANP receptors are modulated by alterations in sodium and fluid intake, and the peptides themselves. Sodium 62-68 angiotensinogen Homo sapiens 5-11 1937678-8 1991 Thus, these individuals have an enhanced adrenal response to Ang II under circumstances in which it should be reduced, thereby leading to lower renin levels and a tendency toward sodium retention. Sodium 179-185 angiotensinogen Homo sapiens 61-67 1937678-9 1991 The second group has the opposite defect; that is, on a low sodium diet, they have a reduced adrenal response to Ang II. Sodium 60-66 angiotensinogen Homo sapiens 113-119 1937678-11 1991 The sodium sensitivity of their blood pressure arises not from the adrenal abnormality but from the associated defect in sodium-dependent, Ang II-mediated changes in renal blood flow. Sodium 4-10 angiotensinogen Homo sapiens 139-145 1937678-11 1991 The sodium sensitivity of their blood pressure arises not from the adrenal abnormality but from the associated defect in sodium-dependent, Ang II-mediated changes in renal blood flow. Sodium 121-127 angiotensinogen Homo sapiens 139-145 1808355-3 1991 Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Sodium 60-66 angiotensinogen Homo sapiens 0-14 1741989-5 1991 Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Sodium 69-75 angiotensinogen Homo sapiens 159-164 1829901-7 1991 Plasma renin activity and plasma angiotensin II levels were significantly lower on LK than on LS or HK, probably reflecting sodium retention. Sodium 124-130 angiotensinogen Homo sapiens 33-47 1851181-6 1991 In the diabetic subjects, however, the responses of plasma 18-OHB and PA to both ACTH injection and graded AII infusions on a 100-mmol, but not on a 170-mmol, sodium intake were subnormal (P less than 0.05 or P less than 0.01) and were similar to those on a 170-mmol sodium intake. Sodium 159-165 angiotensinogen Homo sapiens 107-110 1879402-1 1991 The level of sodium intake has a reciprocal influence on the vascular and adrenal responses to angiotensin II, with sodium restriction enhancing the adrenal responses and reducing vascular, and particularly renal vascular, responses. Sodium 13-19 angiotensinogen Homo sapiens 95-109 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 19-25 angiotensinogen Homo sapiens 119-133 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 19-25 angiotensinogen Homo sapiens 182-196 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 202-208 angiotensinogen Homo sapiens 119-133 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 202-208 angiotensinogen Homo sapiens 182-196 2188439-2 1990 This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. Sodium 189-195 angiotensinogen Homo sapiens 60-73 1799183-5 1991 Both doses of AII decreased GFR and RPF and increased the filtration fraction (FF); the modifications of these parameters, as well as the reduction of FELi and the fractional excretion of sodium (FENa) and the increase of plasma aldosterone and of plasma atrial natriuretic peptide (ANP), were more evident with pressor doses of AII, which increased the blood pressure from 129/83 to 142/95 mm Hg (p less than 0.01). Sodium 188-194 angiotensinogen Homo sapiens 14-17 1799183-8 1991 These results suggest that, in normal humans, the AII-induced rise of FF may be an important factor, even if not the only one, in enhancing the proximal reabsorption of lithium and thus of sodium, whilst it does not affect the absorption of beta 2M. Sodium 189-195 angiotensinogen Homo sapiens 50-53 1886454-1 1991 We examined the possible involvement of angiotensin II in the modulation of circulating norepinephrine produced by acute sodium restriction in essential hypertensive patients (n = 18). Sodium 121-127 angiotensinogen Homo sapiens 40-54 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 171-177 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-6 1991 It can be interpreted that acute sodium depletion results in a substantial contribution of angiotensin II to the expression of hyperadrenergic activity. Sodium 33-39 angiotensinogen Homo sapiens 91-105 2383375-2 1990 Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Sodium 152-158 angiotensinogen Homo sapiens 143-146 2383375-2 1990 Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Sodium 152-158 angiotensinogen Homo sapiens 270-273 2007003-1 1991 There is a growing awareness that the direct intrarenal actions of angiotensin II (ANG II) on both tubular and vascular structures contribute to sodium conservation. Sodium 145-151 angiotensinogen Homo sapiens 67-81 2007003-1 1991 There is a growing awareness that the direct intrarenal actions of angiotensin II (ANG II) on both tubular and vascular structures contribute to sodium conservation. Sodium 145-151 angiotensinogen Homo sapiens 83-89 2007003-9 1991 At these higher doses, the direct hemodynamic actions of ANG II, plus the effects on the glomerular filtration coefficient, will directly reduce filtered sodium load. Sodium 154-160 angiotensinogen Homo sapiens 57-63 2007003-10 1991 Through these synergistic effects on both tubular reabsorptive and hemodynamic function, ANG II can elicit sustained decreases in distal nephron sodium delivery which contribute greatly to its efficacy as a regulator of sodium excretion. Sodium 145-151 angiotensinogen Homo sapiens 89-95 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 angiotensinogen Homo sapiens 66-80 1886454-0 1991 Angiotensin II mediates hyperadrenergic activity evoked by sodium restriction in essential hypertension. Sodium 59-65 angiotensinogen Homo sapiens 0-14 1652115-6 1991 In conclusion, reduced water and sodium excretion after frusemide in the nephrotic syndrome is accompanied by a diminished reduction of blood volume, a delayed decrease in atrial natriuretic peptide, and a blunted increase in angiotensin II and aldosterone compared with healthy subjects. Sodium 33-39 angiotensinogen Homo sapiens 226-240 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 angiotensinogen Homo sapiens 37-51 2167792-0 1990 Role of atrial natriuretic factor in changes in the responsiveness of aldosterone to angiotensin II secondary to sodium loading and depletion in man. Sodium 113-119 angiotensinogen Homo sapiens 85-99 2167792-2 1990 Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. Sodium 0-6 angiotensinogen Homo sapiens 65-79 2383375-1 1990 Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Sodium 0-6 angiotensinogen Homo sapiens 48-62 2383375-1 1990 Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Sodium 0-6 angiotensinogen Homo sapiens 64-67 2185149-0 1990 Angiotensin II: a powerful controller of sodium transport in the early proximal tubule. Sodium 41-47 angiotensinogen Homo sapiens 0-14 2185149-1 1990 Angiotensin II has recently been shown to exert potent control over sodium and water absorption in the proximal convoluted tubule. Sodium 68-74 angiotensinogen Homo sapiens 0-14 2185149-5 1990 These direct tubular transport actions by angiotensin II may participate importantly in various physiological actions of the kidney, including the renal response to change in dietary sodium intake and in extracellular volume, as well as in pathophysiological processes such as hypertension. Sodium 183-189 angiotensinogen Homo sapiens 42-56 2188439-2 1990 This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. Sodium 189-195 angiotensinogen Homo sapiens 104-118 2309737-7 1990 Patients with NIDDM also had augmented blood pressure responses to infused angiotensin II on both sodium diets when compared to control subjects. Sodium 98-104 angiotensinogen Homo sapiens 75-89 2187635-6 1990 Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure. Sodium 64-70 angiotensinogen Homo sapiens 32-46 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 11-25 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 27-33 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 41-47 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 angiotensinogen Homo sapiens 53-67 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 angiotensinogen Homo sapiens 69-72 34180640-5 2021 It will specifically emphasize the "yin-yang" nature of Ang II signaling by comparing and contrasting the effects and activity of various systems, pathways and components found in hypertension to those found in Gitelman"s and Bartter"s syndromes (GS/BS), two rare autosomal recessive tubulopathies characterized by electrolytic imbalance, metabolic alkalosis, sodium wasting and prominent activation of the renin-angiotensin-aldosterone system. Sodium 360-366 angiotensinogen Homo sapiens 56-62 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 273-287 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 289-295 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 63-69 angiotensinogen Homo sapiens 273-287 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 63-69 angiotensinogen Homo sapiens 289-295 34769164-3 2021 This narrative review summarizes the main data dealing with the role of mineralocorticoid and ANG II receptors in the central control of sodium appetite. Sodium 137-143 angiotensinogen Homo sapiens 94-100 34769164-6 2021 Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Sodium 28-34 angiotensinogen Homo sapiens 207-213 34769164-8 2021 ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Sodium 92-98 angiotensinogen Homo sapiens 55-61 34079337-2 2021 The angiotensin I-converting enzyme (ACE1), angiotensin-converting enzyme 2 (ACE2), angiotensinogen (AGT) and receptors angiotensin II receptor type 1 (AGTR1) are key factors for SARS-CoV-2 entering in the cells, sodium and water retention with an increase blood pressure, promotion of fibrotic and inflammatory phenomena resulting in a cytokine storm. Sodium 213-219 angiotensinogen Homo sapiens 84-99 2673301-11 1989 These results suggest that the modulation of the vascular responsiveness to Ang II by prostaglandins is altered by sodium balance and salt sensitivity in EH. Sodium 115-121 angiotensinogen Homo sapiens 76-82 2690611-6 1989 To maintain glomerular filtration rate and an adequate excretion of sodium, the ischemic nephrons require a higher rate of renin secretion than they are actually receiving, because at low perfusion pressures maximal angiotensin II-induced efferent arteriolar constriction is needed to maintain glomerular filtration rate. Sodium 68-74 angiotensinogen Homo sapiens 216-230 2690611-8 1989 This angiotensin II impairs sodium excretion (adaptive hypernatriuresis) from unaffected, adapting nephrons by promoting proximal sodium reabsorption and by inducing afferent constriction. Sodium 28-34 angiotensinogen Homo sapiens 5-19 2690611-8 1989 This angiotensin II impairs sodium excretion (adaptive hypernatriuresis) from unaffected, adapting nephrons by promoting proximal sodium reabsorption and by inducing afferent constriction. Sodium 130-136 angiotensinogen Homo sapiens 5-19 2558135-0 1989 Antihypertensive contribution of sodium depletion and the sympathetic axis during chronic angiotensin II converting enzyme inhibition. Sodium 33-39 angiotensinogen Homo sapiens 90-104 2553328-0 1989 Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension. Sodium 53-59 angiotensinogen Homo sapiens 35-49 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 angiotensinogen Homo sapiens 51-65 2512459-4 1989 Variations in medullary circulation induced by angiotensin II could alter medullary interstitial pressure and the medullary production of prostaglandins E2 and I2 and, ultimately, could modulate sodium reabsorption in the medullary thick ascending limbs and the collecting ducts. Sodium 195-201 angiotensinogen Homo sapiens 47-61 2685117-6 1989 These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses. Sodium 40-46 angiotensinogen Homo sapiens 62-68 2673301-6 1989 The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. Sodium 82-88 angiotensinogen Homo sapiens 42-48 2673301-6 1989 The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. Sodium 108-114 angiotensinogen Homo sapiens 42-48 2673301-7 1989 IND significantly increased the MBP response to Ang II on low sodium intake in NSS and NT, but not in SS. Sodium 62-68 angiotensinogen Homo sapiens 48-54 2673301-8 1989 IND significantly increased the TPR response to Ang II on low sodium intake, remarkably in NSS and NT compared with SS. Sodium 62-68 angiotensinogen Homo sapiens 48-54 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 53-59 angiotensinogen Homo sapiens 127-133 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 148-154 angiotensinogen Homo sapiens 127-133 2673301-10 1989 After captopril administration, IND still increased the MBP and TPR response to Ang II on low sodium intake. Sodium 94-100 angiotensinogen Homo sapiens 80-86 2736884-6 1989 Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 +/- 13 to 82 +/- 10 mumol/min). Sodium 67-73 angiotensinogen Homo sapiens 23-29 2527200-0 1989 Effect of plasma sodium on aldosterone secretion during angiotensin II stimulation in normal humans. Sodium 17-23 angiotensinogen Homo sapiens 56-70 2527200-11 1989 We conclude that small physiological elevations of plasma sodium concentrations can signal substantial decreases of plasma aldosterone in normal human subjects in situations where plasma angiotensin II is moderately elevated. Sodium 58-64 angiotensinogen Homo sapiens 187-201 2757896-4 1989 We have investigated the possible interaction of physiological doses of angiotensin II and noradrenaline on sodium excretion in man. Sodium 108-114 angiotensinogen Homo sapiens 72-86 2757896-12 1989 Angiotensin II when infused with placebo caused a 37% fall in absolute sodium excretion and a 32% fall when infused with noradrenaline (no significant difference between the 2 days). Sodium 71-77 angiotensinogen Homo sapiens 0-14 2736884-12 1989 ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. Sodium 49-55 angiotensinogen Homo sapiens 0-6 2473352-7 1989 The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. Sodium 139-145 angiotensinogen Homo sapiens 42-48 2522705-9 1989 Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption. Sodium 306-312 angiotensinogen Homo sapiens 79-93 2523767-13 1989 The antinatriuretic effects of exogenous AII were reversed by superimposed ANP infusion (urinary sodium excretion: from 4.8 +/- 1.0 to 24.3 +/- 5.2 mEq/h, P less than 0.01). Sodium 97-103 angiotensinogen Homo sapiens 41-44 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 34-40 angiotensinogen Homo sapiens 65-68 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 angiotensinogen Homo sapiens 65-68 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 angiotensinogen Homo sapiens 65-68 2554261-4 1989 The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation. Sodium 91-97 angiotensinogen Homo sapiens 204-218 2655608-2 1989 Angiotensin II (AII) acts as a potent pressor agent directly, by virtue of its vasoconstrictor activity and indirectly, by the volume expansion resulting from stimulation of aldosterone release from the adrenal cortex, leading to sodium and water retention. Sodium 230-236 angiotensinogen Homo sapiens 0-14 2655608-2 1989 Angiotensin II (AII) acts as a potent pressor agent directly, by virtue of its vasoconstrictor activity and indirectly, by the volume expansion resulting from stimulation of aldosterone release from the adrenal cortex, leading to sodium and water retention. Sodium 230-236 angiotensinogen Homo sapiens 16-19 2473352-7 1989 The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. Sodium 139-145 angiotensinogen Homo sapiens 170-176 2473352-8 1989 These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium. Sodium 185-191 angiotensinogen Homo sapiens 39-45 2473352-8 1989 These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium. Sodium 185-191 angiotensinogen Homo sapiens 143-149 2474096-6 1989 Angiotensin II, by its hemodynamic and tubular effects, modulates renal sodium and water excretion and has an important role in blood pressure regulation. Sodium 72-78 angiotensinogen Homo sapiens 0-14 3411123-0 1988 The effects of intravenous angiotensin II upon blood pressure and sodium and urate excretion in human pregnancy. Sodium 66-72 angiotensinogen Homo sapiens 27-41 3292416-8 1988 During sodium restriction, PRA was significantly lower (p less than 0.01) in the sodium-sensitive subsets (2.56 +/- 1.6 vs 4.04 +/- 2.6; 2.65 +/- 2.1 vs 3.88 +/- 2.6 ng angiotensin I/ml/hr). Sodium 81-87 angiotensinogen Homo sapiens 169-182 3292417-8 1988 Interstitial angiotensin II could influence sodium tubular reabsorption directly by stimulating sodium transport in proximal renal tubules and indirectly by altering medullary blood flow and, thereby, medullary interstitial pressure. Sodium 44-50 angiotensinogen Homo sapiens 13-27 3292417-8 1988 Interstitial angiotensin II could influence sodium tubular reabsorption directly by stimulating sodium transport in proximal renal tubules and indirectly by altering medullary blood flow and, thereby, medullary interstitial pressure. Sodium 96-102 angiotensinogen Homo sapiens 13-27 3071591-2 1988 The cerebrospinal fluid concentration of angiotensin II (Ang II) from the patients on a normal-sodium diet was 1.36 +/- 0.41 fmol/ml (n = 5). Sodium 95-101 angiotensinogen Homo sapiens 41-55 3414540-3 1988 When a volume deficit occurs, e.g., by restriction of sodium intake or through hemorrhage, a substantial part of the renal vasoconstriction that occurs is due to angiotensin II. Sodium 54-60 angiotensinogen Homo sapiens 162-176 3411123-6 1988 Angiotensin II evoked a dose-dependent pressor response, a graded increase in PAC and a reduction in sodium and urate excretion in both pregnant and non-pregnant women. Sodium 101-107 angiotensinogen Homo sapiens 0-14 3411123-7 1988 The administration of Ang II had a proportionately greater effect on sodium and urate excretion in non-pregnant than in pregnant women; the pressor response to Ang II was also decreased in the pregnant women. Sodium 69-75 angiotensinogen Homo sapiens 22-28 3064608-2 1988 Because the kidney is both the source of circulating renin and the final determinant of the state of sodium balance, which in turn defines responsiveness to angiotensin II, one might have anticipated substantial interest in the impact of converting enzyme inhibitors on the kidney when these agents were developed. Sodium 101-107 angiotensinogen Homo sapiens 157-171 3037888-3 1987 These are patients with essential hypertension who fail to modulate their renal blood flow and aldosterone responsiveness to angiotensin II when dietary sodium is changed. Sodium 153-159 angiotensinogen Homo sapiens 125-139 3361121-1 1988 Enhanced renal vasoconstriction and renal tubular sodium reabsorption mediated by noradrenaline and angiotensin II (Ang II) have been implicated in the pathogenesis of essential hypertension. Sodium 50-56 angiotensinogen Homo sapiens 100-114 3361121-1 1988 Enhanced renal vasoconstriction and renal tubular sodium reabsorption mediated by noradrenaline and angiotensin II (Ang II) have been implicated in the pathogenesis of essential hypertension. Sodium 50-56 angiotensinogen Homo sapiens 116-122 2821056-11 1987 With angiotensin II, urine volume was also significantly increased by alpha hANP (150 +/- 27 vs. 81 +/- 15 mL/mmol creatinine with placebo; P less than 0.03), and urine sodium excretion doubled. Sodium 169-175 angiotensinogen Homo sapiens 5-19 3623678-1 1987 To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. Sodium 67-73 angiotensinogen Homo sapiens 120-134 3623678-1 1987 To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. Sodium 67-73 angiotensinogen Homo sapiens 136-142 3623678-2 1987 ANG II was also in nine patients with essential hypertension eating a low sodium diet. Sodium 74-80 angiotensinogen Homo sapiens 0-6 3623678-9 1987 The results suggest that in normal subjects increased DBP responses to ANG II, induced by an increase in sodium intake, are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel blocking drugs nifedipine and diltiazem. Sodium 105-111 angiotensinogen Homo sapiens 71-77 3623678-10 1987 In hypertensive patients on a low sodium diet, increased DBP responses to ANG II infusion were blocked by nifedipine, indicating they are at least partly mediated by increased extracellular to intracellular calcium flux. Sodium 34-40 angiotensinogen Homo sapiens 74-80 11538849-1 1988 Angiotensin II (Ang II) induces a marked reduction in renal blood flow at doses well below those required to induce a pressor response, and as blood flow falls there is a decline in glomerular filtration rate and sodium excretion. Sodium 213-219 angiotensinogen Homo sapiens 0-14 11538849-1 1988 Angiotensin II (Ang II) induces a marked reduction in renal blood flow at doses well below those required to induce a pressor response, and as blood flow falls there is a decline in glomerular filtration rate and sodium excretion. Sodium 213-219 angiotensinogen Homo sapiens 16-22 2970179-12 1988 A less pronounced, but significant increase of absolute sodium excretion of the LK was observed in both groups after AT II infusion. Sodium 56-62 angiotensinogen Homo sapiens 117-122 2965232-5 1987 When ANP was administered against a nonpressor background infusion of ANG II, urinary sodium excretion rose from a new lower level (-93 +/- 22 mumol/min) to a rate not significantly different from control (-22 +/- 25 mumol/min). Sodium 86-92 angiotensinogen Homo sapiens 70-76 3039766-6 1987 The increase in plasma AII levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. Sodium 144-150 angiotensinogen Homo sapiens 23-26 3039766-8 1987 Rises in PRA, AII, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Sodium 77-83 angiotensinogen Homo sapiens 14-17 3037891-2 1987 Angiotensin II supported systemic BP by direct systemic vasoconstriction, by facilitating the central and peripheral effects of the sympathetic nervous system, by promoting renal sodium retention by the production of aldosterone, and by increasing total body water by enhancing thirst and the synthesis of vasopressin. Sodium 179-185 angiotensinogen Homo sapiens 0-14 3037893-6 1987 In addition, the direct renal tubular influence of angiotensin II and aldosterone contribute to sodium retention. Sodium 96-102 angiotensinogen Homo sapiens 51-65 3298415-6 1987 The antinatriuretic effect of captopril may be mediated by reduced angiotensin II-mediated sodium excretion, by decreased prostaglandin production, and/or by indirect effects of reduced blood pressure. Sodium 91-97 angiotensinogen Homo sapiens 67-81 3305466-6 1987 At rest as well as during exercise, Aldo rose with increasing ANG II, but the stimulatory effect of ANG II on Aldo was attenuated with higher sodium intake, as estimated from UVNa. Sodium 142-148 angiotensinogen Homo sapiens 100-106 3585223-1 1987 Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Sodium 100-106 angiotensinogen Homo sapiens 82-96 3585223-3 1987 The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. Sodium 131-137 angiotensinogen Homo sapiens 78-92 3035468-7 1987 Renal effects of angiotensin II and aldosterone are responsible for sodium and water retention. Sodium 68-74 angiotensinogen Homo sapiens 17-31 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 angiotensinogen Homo sapiens 61-75 3028957-0 1987 Role of angiotensin II in the hormonal, renal, and electrolyte response to sodium restriction. Sodium 75-81 angiotensinogen Homo sapiens 8-22 3028957-1 1987 Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. Sodium 78-84 angiotensinogen Homo sapiens 21-35 3028957-1 1987 Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. Sodium 78-84 angiotensinogen Homo sapiens 37-43 3028957-5 1987 Conversely, enalapril substantially altered the blood pressure response to ANG II with sodium restriction, completely preventing the reduction in responsiveness. Sodium 87-93 angiotensinogen Homo sapiens 75-81 3536587-2 1986 Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. Sodium 275-281 angiotensinogen Homo sapiens 128-133 3039093-8 1986 It is concluded that acute ANG II blockade has no influence on the vascular resistance in the human forearm, but increases basal SBF in sodium depleted subjects and "paralyses" the vasoconstrictor response to LBNP. Sodium 136-142 angiotensinogen Homo sapiens 27-33 3760114-1 1986 To study the role of calcium movements in mediating the effects of sodium chloride on the response of plasma aldosterone to angiotensin II (AII), we administered calcium channel-blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes before and after AII infusion. Sodium 67-73 angiotensinogen Homo sapiens 124-138 3760114-1 1986 To study the role of calcium movements in mediating the effects of sodium chloride on the response of plasma aldosterone to angiotensin II (AII), we administered calcium channel-blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes before and after AII infusion. Sodium 67-73 angiotensinogen Homo sapiens 140-143 3760114-2 1986 AII was also infused in 13 patients with essential hypertension eating a high sodium diet. Sodium 78-84 angiotensinogen Homo sapiens 0-3 3760114-9 1986 Calcium infusion increased the aldosterone sensitivity to AII during the low sodium diet, but not during the high sodium diet. Sodium 77-83 angiotensinogen Homo sapiens 58-61 3760114-10 1986 The results suggest that in normal subjects, increased plasma aldosterone responses to AII induced by reduction in sodium intake are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel-blocking drugs nifedipine and diltiazem. Sodium 115-121 angiotensinogen Homo sapiens 87-90 3760114-11 1986 In hypertensive patients eating a high sodium diet, increased aldosterone responses to AII infusion were blocked by nifedipine, indicating that they are at least partly mediated by increased extracellular to intracellular calcium flux. Sodium 39-45 angiotensinogen Homo sapiens 87-90 3017033-11 1986 This may be different in states of sodium depletion with reduced vascular effects of AII. Sodium 35-41 angiotensinogen Homo sapiens 85-88 3521337-0 1986 Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation. Sodium 11-17 angiotensinogen Homo sapiens 31-45 3003304-5 1985 These individuals have a defect in the way that sodium intake modifies adrenal and renal vascular responses to angiotensin II, resulting in an abnormality in sodium handling. Sodium 48-54 angiotensinogen Homo sapiens 111-125 3514280-0 1986 Regulation of glomerular filtration rate and sodium excretion by angiotensin II. Sodium 45-51 angiotensinogen Homo sapiens 65-79 3514280-4 1986 The sodium-retaining action of AngII may be due, in part, to constriction of efferent arterioles and to subsequent changes in peritubular capillary physical forces. Sodium 4-10 angiotensinogen Homo sapiens 31-36 3514280-5 1986 However, AngII may also directly stimulate sodium reabsorption in proximal and distal tubules, although the exact site at which AngII increases distal tubular transport is still uncertain. Sodium 43-49 angiotensinogen Homo sapiens 9-14 3514280-7 1986 Thus, the intrarenal effects of AngII provide a mechanism for stabilizing the GFR and excretion of metabolic waste products while causing sodium and water retention, thereby helping to regulate body fluid volumes and arterial pressure. Sodium 138-144 angiotensinogen Homo sapiens 32-37 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 angiotensinogen Homo sapiens 381-395 3953317-3 1986 AII and Aldo were normal before sodium loading and suppressed after saline in PKD patients and controls. Sodium 32-38 angiotensinogen Homo sapiens 0-3 2422491-10 1986 We conclude that enalapril in essential hypertension alleviates the angiotensin-II-mediated abnormalities in renal hemodynamics and sodium excretion. Sodium 132-138 angiotensinogen Homo sapiens 68-82 3003304-5 1985 These individuals have a defect in the way that sodium intake modifies adrenal and renal vascular responses to angiotensin II, resulting in an abnormality in sodium handling. Sodium 158-164 angiotensinogen Homo sapiens 111-125 4030040-7 1985 Although confirmatory data are needed, our findings suggest that moderate sodium restriction enhances aldosterone responsiveness to endogenous angiotensin II and adrenocorticotropic hormone without diminishing the pressor activity of endogenous angiotensin II. Sodium 74-80 angiotensinogen Homo sapiens 143-157 2932646-2 1985 These three functions are continuously regulated by changes in angiotensin II and aldosterone levels in response to wide variations in dietary intake of sodium and potassium. Sodium 153-159 angiotensinogen Homo sapiens 63-77 2412013-1 1985 Infusion of H.261, the inhibitor of human renin in the baboon, lowered blood angiotensin I, plasma angiotensin II, and arterial pressure suggesting that in the sodium-depleted state angiotensin II contributes to the maintenance of arterial pressure. Sodium 160-166 angiotensinogen Homo sapiens 182-196 3893156-2 1985 At low doses, ANG II stimulates sodium (Na) and water absorption from all intestinal areas. Sodium 32-38 angiotensinogen Homo sapiens 14-20 2985655-11 1985 Thus, short-term converting enzyme inhibition corrected abnormalities in sodium-mediated modulation of renal vascular responsiveness to AII. Sodium 73-79 angiotensinogen Homo sapiens 136-139 3899597-3 1985 The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. Sodium 92-98 angiotensinogen Homo sapiens 37-51 3899597-3 1985 The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. Sodium 92-98 angiotensinogen Homo sapiens 128-142 2991371-4 1985 Over a range of sodium intakes from 15 to 200 mmol/day there was a negative correlation between plasma concentration of angiotensin II and receptor site concentration (rs = 0.57, P less than 0.01). Sodium 16-22 angiotensinogen Homo sapiens 120-147 2991371-9 1985 Angiotensin II receptors in platelets respond to changes in sodium intake like receptors in arterial muscle. Sodium 60-66 angiotensinogen Homo sapiens 0-14 3887946-1 1985 Angiotensin II (ANG II) is a powerful effector agent in the regulation of extracellular volume and exerts an important influence on renal sodium excretion. Sodium 138-144 angiotensinogen Homo sapiens 0-14 3887946-1 1985 Angiotensin II (ANG II) is a powerful effector agent in the regulation of extracellular volume and exerts an important influence on renal sodium excretion. Sodium 138-144 angiotensinogen Homo sapiens 16-22 3887946-2 1985 In addition to its effects on aldosterone secretion, ANG II acts directly on the kidney causing retention of sodium at low (physiological) doses and enhanced sodium excretion at high doses. Sodium 109-115 angiotensinogen Homo sapiens 53-59 3887946-2 1985 In addition to its effects on aldosterone secretion, ANG II acts directly on the kidney causing retention of sodium at low (physiological) doses and enhanced sodium excretion at high doses. Sodium 158-164 angiotensinogen Homo sapiens 53-59 3887946-4 1985 Micropuncture and microperfusion studies have demonstrated that proximal tubular sodium and water transport are stimulated by physiological concentrations (10(-12) to 10(-10) M) of ANG II on the peritubular side, whereas higher doses (10(-7) M) cause inhibition. Sodium 81-87 angiotensinogen Homo sapiens 181-187 3887946-8 1985 The data indicate that ANG II binds to receptors on the basolateral cell membrane and alters the rate of entry of sodium through the luminal membrane to increase or decrease, depending on the concentration of peptide. Sodium 114-120 angiotensinogen Homo sapiens 23-29 3881995-4 1985 ANG II caused a significant fall of glomerular filtration rate, renal plasma flow (with an increase in filtration fraction), fractional sodium excretion, and urine output in both studies. Sodium 136-142 angiotensinogen Homo sapiens 0-6 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 53-59 angiotensinogen Homo sapiens 0-14 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 167-173 angiotensinogen Homo sapiens 0-14 3884028-4 1985 This subpressor dose of angiotensin II significantly decreased urine volume, urinary excretion of sodium, chloride and phosphate and distal delivery [(CH2O + CCl)/GFR X 100] in the absence of changes in GFR or distal fractional chloride absorption [CH2O/(CH2O + CCl)]. Sodium 98-104 angiotensinogen Homo sapiens 24-38 3890393-10 1985 A second possibility is a decrease in sodium content of the arteriolar wall with the consequent decrease in vascular response to pressor agents (angiotensin II, catecholamines). Sodium 38-44 angiotensinogen Homo sapiens 145-159 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 64-70 angiotensinogen Homo sapiens 130-133 6100739-1 1984 Previous studies have demonstrated that dopamine inhibits the aldosterone response to angiotensin II in the sodium deplete state in man, but not in the normal sodium balance state. Sodium 108-114 angiotensinogen Homo sapiens 86-100 6100876-10 1984 Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor. Sodium 122-128 angiotensinogen Homo sapiens 173-187 6100876-10 1984 Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor. Sodium 122-128 angiotensinogen Homo sapiens 267-281 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 64-70 angiotensinogen Homo sapiens 164-167 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 179-185 angiotensinogen Homo sapiens 164-167 6328965-6 1984 Both converting enzyme inhibition with captopril and sodium repletion, factors known to decrease endogenous angiotensin II activity, provoked agonist responses to saralasin infusion. Sodium 53-59 angiotensinogen Homo sapiens 108-122 6393932-8 1984 These chronic elevations of angiotensin II directly increase blood pressure and decrease the kidney"s ability to excrete sodium by either a direct renal effect or indirectly by stimulating aldosterone-dependent sodium retention. Sodium 121-127 angiotensinogen Homo sapiens 28-42 6379373-3 1984 Since sodium deficiency is associated with a reduction in renal dopamine formation, we investigated the effect of dopamine on angiotensin II-induced aldosterone secretion in the sodium-depleted state. Sodium 178-184 angiotensinogen Homo sapiens 126-140 6097382-5 1984 Blood pressure response to angiotensin II was greater on the higher sodium intake. Sodium 68-74 angiotensinogen Homo sapiens 27-41 6385344-0 1984 Angiotensin II analogue infusion test in renovascular hypertension under low sodium intake and under spironolactone administration: is angiotensin II analogue infusion test useful in determining the mode of treatment? Sodium 77-83 angiotensinogen Homo sapiens 0-14 6323514-1 1984 Human platelets possess angiotensin II (AII) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal AII receptors. Sodium 95-101 angiotensinogen Homo sapiens 24-38 6323514-1 1984 Human platelets possess angiotensin II (AII) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal AII receptors. Sodium 95-101 angiotensinogen Homo sapiens 40-43 6373591-10 1984 Dopamine inhibits AII-induced aldosterone secretion during sodium deficiency in humans. Sodium 59-65 angiotensinogen Homo sapiens 18-21 6097382-7 1984 Kaliuresis was increased on the day of the 4-h infusion of angiotensin II on the higher sodium intake but no significant changes were apparent during the administration of angiotensin II. Sodium 88-94 angiotensinogen Homo sapiens 59-73 6400108-4 1983 Locally synthetized vasodilatory hormones (kinins, prostaglandins) modulate the effects of angiotensin II (AII), norepinephrine and alpha-adrenergic stimuli on renal vasculature and sodium excretion. Sodium 182-188 angiotensinogen Homo sapiens 91-105 6358261-0 1983 Defect in the sodium-modulated tissue responsiveness to angiotensin II in essential hypertension. Sodium 14-20 angiotensinogen Homo sapiens 56-70 6358261-1 1983 In normal subjects, dietary sodium intake modulates renovascular, adrenal, and pressor responses to infused angiotensin II (AII). Sodium 28-34 angiotensinogen Homo sapiens 108-122 6358261-1 1983 In normal subjects, dietary sodium intake modulates renovascular, adrenal, and pressor responses to infused angiotensin II (AII). Sodium 28-34 angiotensinogen Homo sapiens 124-127 6358261-9 1983 Renal blood flow responses to all AII doses were statistically greater on a high-vs.-low salt diet in the NR (P less than 0.001, chi-square) and normotensives (P = 0.004, chi-square) but sodium intake had no effect on this response in the AbR. Sodium 187-193 angiotensinogen Homo sapiens 34-37 6100600-1 1983 Sodium intake has a substantial effect on target tissue responsiveness to angiotensin II (AII). Sodium 0-6 angiotensinogen Homo sapiens 74-88 6100600-1 1983 Sodium intake has a substantial effect on target tissue responsiveness to angiotensin II (AII). Sodium 0-6 angiotensinogen Homo sapiens 90-93 6100600-3 1983 In a substantial number of patients with essential hypertension this normal sodium-mediated modulation of tissue responsiveness to AII is absent. Sodium 76-82 angiotensinogen Homo sapiens 131-134 6100600-6 1983 The elevated blood pressure may result either from an alteration in renal sodium handling or inappropriate increases in AII levels, depending on ambient sodium intake. Sodium 153-159 angiotensinogen Homo sapiens 120-123 6309884-0 1983 Endogenous angiotensin II as a determinant of sodium-modulated changes in tissue responsiveness to angiotensin II in normal man. Sodium 46-52 angiotensinogen Homo sapiens 11-25 6309884-0 1983 Endogenous angiotensin II as a determinant of sodium-modulated changes in tissue responsiveness to angiotensin II in normal man. Sodium 46-52 angiotensinogen Homo sapiens 99-113 6309884-1 1983 Dietary sodium restriction reduces vascular smooth muscle, particularly renovascular, responsiveness to infused angiotensin II (AII), while the responsiveness of the adrenal and the AII-renin short feedback loop to AII is enhanced. Sodium 8-14 angiotensinogen Homo sapiens 112-126 6309884-1 1983 Dietary sodium restriction reduces vascular smooth muscle, particularly renovascular, responsiveness to infused angiotensin II (AII), while the responsiveness of the adrenal and the AII-renin short feedback loop to AII is enhanced. Sodium 8-14 angiotensinogen Homo sapiens 128-131 6309884-5 1983 In sodium-restricted subjects, preinfusion AII and aldosterone levels were significantly reduced, (P less than 0.001) to the range found in sodium-replete subjects, after 75 h of MK421 administration, whereas blood pressure and PAH responses to infused AII were significantly enhanced (P less than 0.01). Sodium 3-9 angiotensinogen Homo sapiens 43-46 6309884-6 1983 Blood pressure and PAH responses to infused AII in sodium-replete subjects were not significantly modified by MK421 treatment, confirming that the drug effect was specific. Sodium 51-57 angiotensinogen Homo sapiens 44-47 6309884-8 1983 Thus, sodium-modulated changes in PAH and blood pressure responsiveness to infused AII depend on circulating AII levels. Sodium 6-12 angiotensinogen Homo sapiens 83-86 6309884-8 1983 Thus, sodium-modulated changes in PAH and blood pressure responsiveness to infused AII depend on circulating AII levels. Sodium 6-12 angiotensinogen Homo sapiens 109-112 6309884-10 1983 Two different mechanisms determine sodium modulation of tissue responsiveness to AII; in one, circulating AII via a receptor mechanism is the mediator, and in the other, some other factor(s) also linked to sodium intake must be responsible. Sodium 35-41 angiotensinogen Homo sapiens 81-84 6309884-10 1983 Two different mechanisms determine sodium modulation of tissue responsiveness to AII; in one, circulating AII via a receptor mechanism is the mediator, and in the other, some other factor(s) also linked to sodium intake must be responsible. Sodium 35-41 angiotensinogen Homo sapiens 106-109 6883736-7 1983 A significant inverse relationship existed between sodium intake and bioactive angiotensin II in 5 normal subjects studied on low, normal and high sodium diets. Sodium 51-57 angiotensinogen Homo sapiens 79-93 6366501-0 1983 A comparison of biological effects of three angiotensin II antagonists in sodium depleted hypertensive patients. Sodium 74-80 angiotensinogen Homo sapiens 44-58 6341220-6 1983 The increase in RVR in response to AII was positively correlated to sodium intake and plasma aldosterone concentration, indicating that these two factors might modulate the renal vascular reactivity. Sodium 68-74 angiotensinogen Homo sapiens 35-38 6310234-6 1983 Angiotensin II infusion in both sodium replete and deplete states also caused variable aldosterone responses. Sodium 32-38 angiotensinogen Homo sapiens 0-14 6343958-8 1983 A marked increase of the production of Angiotensin-I with increasing sodium concentrations at a low Potassium range was observed and the opposite was true at high Potassium concentrations. Sodium 69-75 angiotensinogen Homo sapiens 39-52 6822640-10 1983 These results suggest that dopamine may be an important regulator of the alterations in aldosterone responsiveness to AII that occur during changes in dietary sodium intake. Sodium 159-165 angiotensinogen Homo sapiens 118-121 6625420-4 1983 Sodium inflation is likely to be responsible for abnormal responses to angiotensin II and its antagonists in normotensive acromegalics, which make the use of these agents inappropriate for the study of the renin-angiotensin-aldosterone system. Sodium 0-6 angiotensinogen Homo sapiens 71-85 6295691-5 1983 Further incremental and percentage changes of 18-OHB in response to graded dose infusions of angiotensin II and adrenocorticotropic hormone (ACTH) were greater during the 40 mmol of sodium intake period. Sodium 182-188 angiotensinogen Homo sapiens 93-139 6822640-0 1983 Dopaminergic modulation of aldosterone responsiveness to angiotensin II with changes in sodium intake. Sodium 88-94 angiotensinogen Homo sapiens 57-71 6822640-1 1983 The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Sodium 71-77 angiotensinogen Homo sapiens 36-50 6822640-1 1983 The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Sodium 71-77 angiotensinogen Homo sapiens 52-55 6183031-1 1982 Animal data suggest that angiotensin II may directly affect renal sodium retention independent of aldosterone (4,6). Sodium 66-72 angiotensinogen Homo sapiens 25-39 6280473-2 1982 On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II. Sodium 7-13 angiotensinogen Homo sapiens 206-220 6175971-0 1982 Intracerebroventricular infusions of angiotensin II increases sodium excretion. Sodium 62-68 angiotensinogen Homo sapiens 37-51 6183031-3 1982 We describe here experiments designed to elucidate the role of angiotensin II in renal sodium retention in normal man. Sodium 87-93 angiotensinogen Homo sapiens 63-77 7018813-11 1981 The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. Sodium 169-175 angiotensinogen Homo sapiens 159-165 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 91-97 angiotensinogen Homo sapiens 7-13 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 91-97 angiotensinogen Homo sapiens 61-67 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 149-155 angiotensinogen Homo sapiens 7-13 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 100-106 angiotensinogen Homo sapiens 7-13 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 100-106 angiotensinogen Homo sapiens 69-75 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 157-163 angiotensinogen Homo sapiens 69-75 7026131-13 1981 The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. Sodium 29-35 angiotensinogen Homo sapiens 199-205 7016959-0 1981 Plasma aldosterone response to angiotensin II in sodium-restricted elderly subjects with essential hypertension. Sodium 49-55 angiotensinogen Homo sapiens 31-45 7047005-5 1982 Apparently some LREH subjects, whose delta PA/delta PRA ratios after sodium restriction were high, have an abnormally enhanced aldosterone responsiveness to AII under the condition of low sodium intake. Sodium 69-75 angiotensinogen Homo sapiens 157-160 7047005-5 1982 Apparently some LREH subjects, whose delta PA/delta PRA ratios after sodium restriction were high, have an abnormally enhanced aldosterone responsiveness to AII under the condition of low sodium intake. Sodium 188-194 angiotensinogen Homo sapiens 157-160 7077947-1 1982 Changes in renal hemodynamics and sodium excretion induced by an angiotensin II (AII) infusion were correlated with urinary prostaglandin E2 (PGE2) excretion in 15 patients with cirrhosis and ascites. Sodium 34-40 angiotensinogen Homo sapiens 65-79 7077947-1 1982 Changes in renal hemodynamics and sodium excretion induced by an angiotensin II (AII) infusion were correlated with urinary prostaglandin E2 (PGE2) excretion in 15 patients with cirrhosis and ascites. Sodium 34-40 angiotensinogen Homo sapiens 81-84 7077947-10 1982 We conclude that in patients with hepatic cirrhosis, the sodium excretion pattern induced by an exogenous AII challenge may depend on the prior state of intrarenal prostaglandin activity. Sodium 57-63 angiotensinogen Homo sapiens 106-109 7026131-0 1981 Plasma angiotensin II concentration regulates vascular but not adrenal responsiveness to restriction of sodium intake in normal man. Sodium 104-110 angiotensinogen Homo sapiens 7-21 7026131-2 1981 Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 75-89 7026131-2 1981 Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 91-97 6114434-2 1981 Angiotensin II also mediates the adrenal effects of altered sodium balance, and is essential for the aldosterone response to sodium restriction. Sodium 60-66 angiotensinogen Homo sapiens 0-14 6114434-2 1981 Angiotensin II also mediates the adrenal effects of altered sodium balance, and is essential for the aldosterone response to sodium restriction. Sodium 125-131 angiotensinogen Homo sapiens 0-14 6114434-3 1981 However, the adrenal effects of angiotensin II are attenuated during sodium loading, suggesting that other local or humoral factors modulate its actions on adrenal glomerulosa function. Sodium 69-75 angiotensinogen Homo sapiens 32-46 7016959-7 1981 Apparently some subjects with essential hypertension, whose PRAs response subnormally to sodium restriction, have an abnormally enhanced adrenal responsiveness to AII under the conditions of low-sodium intake. Sodium 89-95 angiotensinogen Homo sapiens 163-166 7016959-7 1981 Apparently some subjects with essential hypertension, whose PRAs response subnormally to sodium restriction, have an abnormally enhanced adrenal responsiveness to AII under the conditions of low-sodium intake. Sodium 195-201 angiotensinogen Homo sapiens 163-166 7211097-2 1981 We investigated whether the "sensitization" of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. Sodium 101-107 angiotensinogen Homo sapiens 76-90 7211097-2 1981 We investigated whether the "sensitization" of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. Sodium 101-107 angiotensinogen Homo sapiens 92-96 7211097-5 1981 In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although "sensitization" was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Sodium 75-81 angiotensinogen Homo sapiens 42-46 6258080-3 1981 The positive regulatory action of angiotensin II on its adrenal receptors occurs with elevations of the circulating peptide concentration within the physiological range and probably contributes to the increased sensitivity of the adrenal during sodium deficiency. Sodium 245-251 angiotensinogen Homo sapiens 34-48 7009427-1 1981 Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery. Sodium 45-51 angiotensinogen Homo sapiens 21-35 7266710-6 1981 With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. Sodium 217-223 angiotensinogen Homo sapiens 35-49 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 angiotensinogen Homo sapiens 98-112 7428699-0 1980 Stimulation of intestinal sodium and water transport in vivo by angiotensin II and analogs. Sodium 26-32 angiotensinogen Homo sapiens 64-78 7193170-6 1980 These findings are tentatively explained by two mechanisms: 1) Angiotensin II has a "trophic" effect on the adrenal cortex, thus causing a progressive increase of secretion of corticosteroids in the normal sodium as well as in the low sodium state. Sodium 206-212 angiotensinogen Homo sapiens 63-77 6253796-2 1980 Elevation of circulating angiotensin II levels by sodium depletion or renal artery stenosis is associated with a diminished pressor response to infused angiotensin II (refs 1-3). Sodium 50-56 angiotensinogen Homo sapiens 25-39 6253796-2 1980 Elevation of circulating angiotensin II levels by sodium depletion or renal artery stenosis is associated with a diminished pressor response to infused angiotensin II (refs 1-3). Sodium 50-56 angiotensinogen Homo sapiens 152-166 6253796-3 1980 Conversely, the vasocontrictor response to the hormone is enhanced when endogenous angiotensin II levels are reduced by sodium loading or nephrectomy. Sodium 120-126 angiotensinogen Homo sapiens 83-97 6156899-3 1980 With restriction of sodium intake, an increase in renal blood flow occurs; because a quantitatively similar response occurs to the angiotensin II analogs it is likely that the response reflects reversal of the local action of angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 226-240 6988802-2 1980 For a daily sodium intake of 120 mmol plasma angiotensinogen was abnormally increased, plasma renin activity (PRA) remained normal, but without significant diurnal variation. Sodium 12-18 angiotensinogen Homo sapiens 45-60 7470759-5 1980 The falls in absolute and fractional sodium excretions caused by this manoeuvre were of similar magnitude to those obtained in the absence of drug.5 The results obtained using the 1-Sar, 8-Ile angiotensin II are consistent with angiotensin II having an important intra-renal site of action to regulate glomerular filtration rate, possibly via an action at the efferent arteriole. Sodium 37-43 angiotensinogen Homo sapiens 228-242 90271-2 1979 Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Sodium 78-84 angiotensinogen Homo sapiens 7-21 397605-2 1979 Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. Sodium 212-218 angiotensinogen Homo sapiens 95-109 531273-7 1979 This observation indicates that S, like angiotensin II, has a direct effect upon the renal tubules evoking an increase of sodium reabsorption. Sodium 122-128 angiotensinogen Homo sapiens 40-54 455738-3 1979 It is concluded that angiotensin II plays a major part in stimulating aldosterone secretion during sodium depletion in man. Sodium 99-105 angiotensinogen Homo sapiens 21-35 699348-3 1978 Deprivation of sodium without bromocriptine resulted in progressive and highly significant increases in the plasma concentration of aldosterone from 230 +/- 50 to 418 +/- 44 (SEM) pmol/l, 18-hydroxycorticosterone from 627 +/- 138 to 1420 +/- 478 pmol/l, PRC from 108 +/- 38 to 166 +/- 14 muU/ml and AII from 16 +/- 3 to 29 +/- 4 pmol/l. Sodium 15-21 angiotensinogen Homo sapiens 299-302 289865-0 1979 Angiotensin II blockade: evidence for baroreceptor-mediated renin release and the role of sodium balance. Sodium 90-96 angiotensinogen Homo sapiens 0-14 474181-3 1979 AII was then correlated statistically to PRA, PA and 24-hour urinary excretions of aldosterone (Aldo-U), sodium and potassium and to the blood pressure (BP) levels. Sodium 105-111 angiotensinogen Homo sapiens 0-3 30650-4 1978 Recently, it has been shown that angiotensin II, infused intravenously or through the carotid artery at rates that produce increases in plasma angiotensin II levels similar to those that occur in mild sodium depletion, causes the water-replete animal to drink. Sodium 201-207 angiotensinogen Homo sapiens 33-47 30650-4 1978 Recently, it has been shown that angiotensin II, infused intravenously or through the carotid artery at rates that produce increases in plasma angiotensin II levels similar to those that occur in mild sodium depletion, causes the water-replete animal to drink. Sodium 201-207 angiotensinogen Homo sapiens 143-157 699348-5 1978 Sodium deprivation together with bromocriptine resulted in increases in the plasma concentrations of aldosterone from 230 +/- 47 to 416 +/- 72 pmol/l, 18-hydroxycorticosterone from 630 +/- 99 to 1629 +/- 552 pmol/l, PRC from 105 +/- 12 muU/ml and AII from 14 +/- 3 to 26 +/- 5 pmol/l. Sodium 0-6 angiotensinogen Homo sapiens 247-250 672437-0 1978 Comparison of the biological effects of two angiotensin II analogues in hypertensive patients with sodium depletion. Sodium 99-105 angiotensinogen Homo sapiens 44-58 233670-1 1978 A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Sodium 172-178 angiotensinogen Homo sapiens 56-70 233670-1 1978 A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Sodium 172-178 angiotensinogen Homo sapiens 72-75 701125-6 1978 Angiotensin II may thus have a role in the maintenance of P- in the supine sodium-deplete normal subjects, and stimulation of the renin angiotensin system during physical exercise contributes to a minor extent to the increase in P- in these conditions. Sodium 75-81 angiotensinogen Homo sapiens 0-14 699587-3 1978 Conceivably saralasin exerts different sodium-dependent effects on peripheral angiotensin II and specific intrarenal vascular receptors. Sodium 39-45 angiotensinogen Homo sapiens 78-92 642412-5 1978 Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium. Sodium 7-13 angiotensinogen Homo sapiens 52-57 221518-0 1978 Prolonged infusions of Ile5-angiotensin-II in sodium replete and deplete man: effects on aldosterone, ACTH, cortisol, blood pressure, and electrolyte balance. Sodium 46-52 angiotensinogen Homo sapiens 28-42 221518-1 1978 Angiotensin II (Ile5) was infused for 72 h into 4 sodium replete (3 ng/kg/min) and 8 sodium deplete (3 or 6 ng/kg/min) healthy young men after appropriate control periods, and the effects on aldosterone secretion, plasma cortisol, ACTH, renin activity, plasma and urinary electrolytes, and blood pressure were assessed. Sodium 50-56 angiotensinogen Homo sapiens 0-14 221518-2 1978 Sustained contrived elevation of plasma angiotensin II levels in sodium replete subjects to the range of moderate sodium depletion led to a sustained increase in plasma and urinary aldosterone levels, which further and significantly increased between the 1st and 2nd days of angiotensin II infusion, when gross sodium retention during infusion was prevented. Sodium 65-71 angiotensinogen Homo sapiens 40-54 221518-4 1978 In the sodium deplete state, the absolute increment of aldosterone secretion for a given elevation of angiotensin II levels diring infusion was larger than in sodium replete subjects. Sodium 7-13 angiotensinogen Homo sapiens 102-116 221518-5 1978 This confirms the conclusions from previous short-term angiotensin II infusion experiments that sodium deficiency sensitizes the zona glomerulosa against angiotensin II. Sodium 96-102 angiotensinogen Homo sapiens 55-69 221518-5 1978 This confirms the conclusions from previous short-term angiotensin II infusion experiments that sodium deficiency sensitizes the zona glomerulosa against angiotensin II. Sodium 96-102 angiotensinogen Homo sapiens 154-168 221518-9 1978 The opposite shifts in sensitivity against angiotensin II of the zona glomerulosa and of resistance blood vessels with changes in the sodium state seem to be an effective and important means in the regulation of body sodium. Sodium 134-140 angiotensinogen Homo sapiens 43-57 735881-8 1978 Angiotensin II appears to be of importance for the maintenance of BP in sodium replete hypertensive patients with normal or high PRA. Sodium 72-78 angiotensinogen Homo sapiens 0-14 902672-3 1977 The combined hypotensive response to acute sodium volume depletion and to angiotensin II blockade during sodium volume depletion was not related to PRC (r = 0.15; p greater than 0.1). Sodium 105-111 angiotensinogen Homo sapiens 74-88 920808-0 1977 Effects of endogenous angiotensin II on renal sodium excretion and renal hemodynamics. Sodium 46-52 angiotensinogen Homo sapiens 22-36 601775-6 1977 The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet. Sodium 143-149 angiotensinogen Homo sapiens 30-44 628191-0 1978 Effect of prolonged low-dose infusions of ile5-angiotensin ii on blood pressure, aldosterone and electrolyte excretion in sodium replete man. Sodium 122-128 angiotensinogen Homo sapiens 47-61 628191-2 1978 Plasma angiotensin II levels were therby raised to the range of moderate sodium depletion. Sodium 73-79 angiotensinogen Homo sapiens 7-21 628191-8 1978 Blood pressure increased gradually during angiotensin II infusion, reflecting changes in sodium balance. Sodium 89-95 angiotensinogen Homo sapiens 42-56 846071-10 1977 These results suggest that angiotensin II plays an active role in sustaining normal blood pressure only under conditions of considerable sodium-depletion. Sodium 137-143 angiotensinogen Homo sapiens 27-41 909130-11 1977 Furthermore, the change in mean arterial pressure induced by infusion of angiotensin II analogue seemed to correlate with DBH activity change by sodium depletion. Sodium 145-151 angiotensinogen Homo sapiens 73-87 874056-2 1977 Significant angiotensin II-dependence of blood pressure was found only after the combined stimulus of sodium restriction (10 mEq daily for 4 days) and ambulation. Sodium 102-108 angiotensinogen Homo sapiens 12-26 870773-9 1977 In a separate study, the adrenal response to infused angiotensin II was determined in 12 hypertensive patients who were on a sodium intake of 200 meq. Sodium 125-131 angiotensinogen Homo sapiens 53-67 870773-12 1977 Thus, some patients with normal-renin essential hypertension may have either enhanced or reduced adrenal responsiveness to angiotensin II, depending on the conditions of dietary intake of sodium. Sodium 188-194 angiotensinogen Homo sapiens 123-137 791534-3 1976 These studies indicate that angiotensin II does not have an obligatory role in blood pressure maintenance in the normal, sodium replete individual, but it is essential following sodium depletion. Sodium 178-184 angiotensinogen Homo sapiens 28-42 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 angiotensinogen Homo sapiens 128-142 791534-4 1976 The role of angiotensin II in feedback control of renin secretion is confirmed as is its importance in aldosterone stimulation both in relation to posture and sodium depletion. Sodium 159-165 angiotensinogen Homo sapiens 12-26 995500-9 1976 A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Sodium 45-51 angiotensinogen Homo sapiens 0-4 1071606-6 1976 These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b)normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake);(c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients. Sodium 60-66 angiotensinogen Homo sapiens 95-109 995500-9 1976 A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Sodium 98-104 angiotensinogen Homo sapiens 0-4 954369-0 1976 Letter: Sodium balance and responsiveness to angiotensin II. Sodium 8-14 angiotensinogen Homo sapiens 45-59 939003-2 1976 Angiotensin II, infused intravenously, increased plasma aldosterone concentration in two of six anephric subjects taking their usual dietary quantities of sodium. Sodium 155-161 angiotensinogen Homo sapiens 0-14 939003-3 1976 After 3 days of dietary sodium restriction and weight-reducing hemodialysis, the aldosterone response to infused angiotensin II in the two previously reactive subjects was enhanced, while the four previously unreactive subjects also showed a rise in plasma aldosterone. Sodium 24-30 angiotensinogen Homo sapiens 113-127 185902-2 1976 A reciprocal relationship exists between sodium balance and the circulating levels of renin and angiotensin II. Sodium 41-47 angiotensinogen Homo sapiens 96-110 185902-3 1976 The vascular responsiveness to angiotensin II, the major vasconstrictor component of the renal pressor system, can be impaired by numerous factors including sodium depletion or a reduction in effective plasma volume. Sodium 157-163 angiotensinogen Homo sapiens 31-45 185902-8 1976 These observations support the view that the decrease in vascular response to angiotensin II during sodium deprivation or when body fluid volumes are reduced is the result of prior occupancy of the receptor sites by endogenous hormone generated both in the plasma and locally within blood vessel walls. Sodium 100-106 angiotensinogen Homo sapiens 78-92 1024254-3 1976 Sodium supply was proved to influence significantly the pressor response to angiotensin II and not that to noradrenaline thus implying the presence of arterial receptors which bind angiotensin specifically. Sodium 0-6 angiotensinogen Homo sapiens 76-90 948620-9 1976 Pressor infusions of angiotensin II raise peripheral levels of IR-PGA, and this response is exaggerated by a low sodium diet and blocked by either acute or chronic indomethacin administration. Sodium 113-119 angiotensinogen Homo sapiens 21-35 174834-5 1976 When converting enzyme inhibitor was administered, which blocked the generation of angiotensin II, sodium replete subjects were able to compensate for an upright tilt, despite the absence of angiotensin II, without significant hemodynamic change when compared to control state. Sodium 99-105 angiotensinogen Homo sapiens 83-97 174834-12 1976 These results indicate that angiotensin II is essential for blood pressure maintenance in sodium depleted individuals, that angiotensin II exerts a direct feedback control on renin secretion, and that angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and to posture. Sodium 90-96 angiotensinogen Homo sapiens 28-42 1255070-0 1976 Proceedings: Relationship between angiotensin II and sodium status in the control of blood pressure: studies in anephric subjects and in subjects with renal hypertension. Sodium 53-59 angiotensinogen Homo sapiens 34-48 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 angiotensinogen Homo sapiens 200-214 1244226-6 1976 Moreover, the oral contraceptive agents modified the basic relationship between sodium balance and vascular responsiveness to angiotensin II, suggesting that the agents acted through some mechanism other than alteration in the state of sodium balance. Sodium 80-86 angiotensinogen Homo sapiens 126-140 1177406-0 1975 [Metabolism of angiotensin II during angiotensin infusion and following sodium depletion]. Sodium 72-78 angiotensinogen Homo sapiens 15-29 798204-6 1976 (a) Prevention of AII generation by nephrectomy or converting enzyme inhibition increases the pressor response to AII which then becomes independent of sodium balance. Sodium 152-158 angiotensinogen Homo sapiens 18-21 1019161-3 1976 2) In standing normotensive volunteers, angiotensin II inhibition induced significant hypotension if previously a cumulative sodium loss of at least 160-200 mEq had been induced. Sodium 125-131 angiotensinogen Homo sapiens 40-54 1177406-10 1975 During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. Sodium 155-161 angiotensinogen Homo sapiens 19-33 1102803-0 1975 Inter-relationships between plasma angiotensin II, arterial pressure, aldosterone and exchangeable sodium in normotensive and hypertensive man. Sodium 99-105 angiotensinogen Homo sapiens 35-49 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 33-47 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 33-47 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 127-141 235559-19 1975 Conversely, in sodium-loaded individuals, assumption of upright posture leads to a parallel rise in A II, TPRA, and bradykinin. Sodium 15-21 angiotensinogen Homo sapiens 100-104 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 angiotensinogen Homo sapiens 102-116 234604-10 1975 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. Sodium 81-87 angiotensinogen Homo sapiens 15-29 4365595-2 1974 We have assessed the effect of decreased sodium intake on their responses to A II in man. Sodium 41-47 angiotensinogen Homo sapiens 77-81 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 angiotensinogen Homo sapiens 240-254 234853-0 1975 Enhancement of the blood pressure activity of VAL5-and ILE5-angiotensin II by sodium and calcium ions. Sodium 78-84 angiotensinogen Homo sapiens 60-74 4365595-9 1974 Sodium restriction reduced the pressor (P < 0.01) and the renal vascular response (P < 0.01), but potentiated the adrenal response to A II (P < 0.01). Sodium 0-6 angiotensinogen Homo sapiens 140-144 4365595-11 1974 Thus, sodium intake reciprocally influences vascular and adrenal responses to A II: salt restriction blunts the vascular response and potentiates the adrenal"s, a physiologically important influence in view of aldosterone"s role in sodium conservation. Sodium 6-12 angiotensinogen Homo sapiens 78-82 4367700-0 1974 [Influence of angiotensin II-infusion on the sodium- and potassium level in plasma and erythrocytes of normotensive persons and patients with essential hypertension (author"s transl)]. Sodium 45-51 angiotensinogen Homo sapiens 14-28 4365595-11 1974 Thus, sodium intake reciprocally influences vascular and adrenal responses to A II: salt restriction blunts the vascular response and potentiates the adrenal"s, a physiologically important influence in view of aldosterone"s role in sodium conservation. Sodium 232-238 angiotensinogen Homo sapiens 78-82 4347443-0 1972 Effect of chlorothiazide and sodium on vascular responsiveness to angiotensin II. Sodium 29-35 angiotensinogen Homo sapiens 66-80 4377498-0 1974 Effect of a competitive antagonist (8-leu-angiotensin II) of angiotensin II on sodium and water transport in toad skin. Sodium 79-85 angiotensinogen Homo sapiens 42-56 4377498-0 1974 Effect of a competitive antagonist (8-leu-angiotensin II) of angiotensin II on sodium and water transport in toad skin. Sodium 79-85 angiotensinogen Homo sapiens 61-75 4359751-0 1974 Proceedings: Pressor sensitivity to angiotensin II in relation to sodium. Sodium 66-72 angiotensinogen Homo sapiens 36-50 4341479-0 1972 Metabolism of angiotensin II in sodium depletion and hypertension in humans. Sodium 32-38 angiotensinogen Homo sapiens 14-28 4117201-0 1972 Raised plasma angiotensin II and aldosterone during dietary sodium restriction in man. Sodium 60-66 angiotensinogen Homo sapiens 14-28 4317871-0 1970 Effect of change of sodium balance on the corticosteroid response to angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 69-83 4108268-0 1971 Circulating angiotensin-II and aldosterone levels during dietary sodium restriction. Sodium 65-71 angiotensinogen Homo sapiens 12-26 4322475-0 1971 The dissociation of aldosterone secretion and systemic renin and angiotensin II levels during the correction of sodium deficiency. Sodium 112-118 angiotensinogen Homo sapiens 65-79 4349531-0 1973 Angiotensin I conversion in the kidney and its modulation by sodium balance. Sodium 61-67 angiotensinogen Homo sapiens 0-13 4337697-0 1972 Effect of angiotensin II on urinary magnesium, calcium, and sodium excretion in normal subjects. Sodium 60-66 angiotensinogen Homo sapiens 10-24 4331448-0 1970 [Effect differences between angiotensin II and noradrenalin in reference to diuresis, sodium and potassium excretion in healthy persons and patients with kidney diseases]. Sodium 86-92 angiotensinogen Homo sapiens 28-42 4302904-0 1968 Effect of angiotensin II on urinary sodium excretion in normal subjects and in cirrhotic patients. Sodium 36-42 angiotensinogen Homo sapiens 10-24 4284773-0 1965 Effect of variations of plasma sodium concentration on the adrenal response to angiotensin II. Sodium 31-37 angiotensinogen Homo sapiens 79-93 4286529-0 1965 Effect of angiotensin II on active transport of sodium by toad bladder and skin. Sodium 48-54 angiotensinogen Homo sapiens 10-24 4300463-0 1968 [Relation between the blood-pressure effect of angiotensin II and the mean arterial pressure, serum sodium, serum potassium, serum angiotensinase and plasma renin in man]. Sodium 100-106 angiotensinogen Homo sapiens 47-61 4285879-0 1966 [Influence of intravenous perfusion of angiotensin II on the urinary elimination of sodium in edematous cardiac patients]. Sodium 84-90 angiotensinogen Homo sapiens 39-53 33028070-1 2021 Background/Aims: This study aimed to investigate whether urinary angiotensinogen (UAGT) excretion was associated with elevated blood pressure in patients with chronic kidney disease (CKD) and to evaluate the relationship among blood pressure, intra-renal renin-angiotensin system (RAS) activity, and dietary sodium in patients with CKD. Sodium 308-314 angiotensinogen Homo sapiens 65-80 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 angiotensinogen Homo sapiens 195-199 32909725-4 2020 These findings are consistent with abnormally increased renal sodium reabsorption, possibly caused by increased angiotensin II activity secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced downregulation of angiotensin-converting enzyme 2 (ACE2) receptors. Sodium 62-68 angiotensinogen Homo sapiens 112-126 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 angiotensinogen Homo sapiens 55-69 32079768-3 2020 Compared with other ligands, AngII promotes more-substantial rearrangements not only at the bottom of the ligand-binding pocket but also in a key polar network in the receptor core, which forms a sodium-binding site in most GPCRs. Sodium 196-202 angiotensinogen Homo sapiens 29-34 31237219-5 2020 RESULTS: Angiotensin II (ANG II), beside stimulating aldosterone, vasopressin and CRH-ACTH release, sodium and water retention, thirst, and sympathetic nerve activity, exerts its effects on the immune system via the Angiotensin Type 1 Receptor (AT 1R) that is located in the brain, pituitary adrenal gland, and kidney. Sodium 100-106 angiotensinogen Homo sapiens 9-23 31237219-5 2020 RESULTS: Angiotensin II (ANG II), beside stimulating aldosterone, vasopressin and CRH-ACTH release, sodium and water retention, thirst, and sympathetic nerve activity, exerts its effects on the immune system via the Angiotensin Type 1 Receptor (AT 1R) that is located in the brain, pituitary adrenal gland, and kidney. Sodium 100-106 angiotensinogen Homo sapiens 25-31 31015582-3 2019 Factors that contribute to increased sodium reabsorption in obesity include kidney compression by visceral, perirenal and renal sinus fat; increased renal sympathetic nerve activity (RSNA); increased levels of anti-natriuretic hormones, such as angiotensin II and aldosterone; and adipokines, particularly leptin. Sodium 37-43 angiotensinogen Homo sapiens 245-259 30803087-1 2019 Angiotensin II (Ang II) acts on Ang II type 1 (AT1) receptors located in the organum vasculosum and subfornical organ (SFO) of the lamina terminalis as a main facilitatory mechanism of sodium appetite. Sodium 185-191 angiotensinogen Homo sapiens 0-23 31129252-2 2019 Angiotensin II and aldosterone are the two most powerful biologically active products of the RAAS, inducing all of the classical actions of the RAAS including vasoconstriction, sodium retention, tissue remodeling and pro-inflammatory and pro-fibrotic effects. Sodium 177-183 angiotensinogen Homo sapiens 0-14 30405294-10 2018 Conclusions: Ang II contributes to sodium retention in retainers. Sodium 35-41 angiotensinogen Homo sapiens 13-19 31061349-2 2019 The vasopressor effects of Ang II include direct contraction of myocardium and vascular smooth muscles (SMs) along with aldosterone-mediated sodium retention. Sodium 141-147 angiotensinogen Homo sapiens 27-33 30839176-1 2019 Sodium transport in the thick ascending loop of Henle (TAL) is tightly regulated by numerous factors, especially angiotensin II (Ang II), a key end-product of the renin-angiotensin system (RAS). Sodium 0-6 angiotensinogen Homo sapiens 113-127 30839176-1 2019 Sodium transport in the thick ascending loop of Henle (TAL) is tightly regulated by numerous factors, especially angiotensin II (Ang II), a key end-product of the renin-angiotensin system (RAS). Sodium 0-6 angiotensinogen Homo sapiens 129-135 29944390-8 2018 In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 +- 94.7 vs. 1,151.7 +- 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 +- 213.9 vs. 1,095.2 +- 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. Sodium 146-152 angiotensinogen Homo sapiens 17-23 29944390-8 2018 In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 +- 94.7 vs. 1,151.7 +- 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 +- 213.9 vs. 1,095.2 +- 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. Sodium 237-243 angiotensinogen Homo sapiens 17-23 29556787-6 2018 Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Sodium 214-220 angiotensinogen Homo sapiens 35-41 28592435-8 2018 The adrenal response to exogenous angiotensin II was significantly lower in men than in women on both sodium intakes. Sodium 102-108 angiotensinogen Homo sapiens 34-48 29378857-3 2018 We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Sodium 47-53 angiotensinogen Homo sapiens 125-139 29045337-5 2018 RECENT FINDINGS: A variety of investigative approaches have demonstrated that angiotensin II signaling via AT1a receptors, specifically in the renal proximal tubule, is a major regulator of BP and sodium homeostasis. Sodium 197-203 angiotensinogen Homo sapiens 78-92 28384411-1 2017 The renin-angiotensin system (RAS) generates, maintains, and makes worse hypertension and cardiovascular diseases (CVDs) through its biologically active component angiotensin II (Ang II), that causes vasoconstriction, sodium retention, and structural alterations of the heart and the arteries. Sodium 218-224 angiotensinogen Homo sapiens 163-177 28384411-1 2017 The renin-angiotensin system (RAS) generates, maintains, and makes worse hypertension and cardiovascular diseases (CVDs) through its biologically active component angiotensin II (Ang II), that causes vasoconstriction, sodium retention, and structural alterations of the heart and the arteries. Sodium 218-224 angiotensinogen Homo sapiens 179-185 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensinogen Homo sapiens 74-88 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensinogen Homo sapiens 90-96 28836382-2 2017 The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in sodium appetite. Sodium 160-166 angiotensinogen Homo sapiens 132-138 28836382-7 2017 This result indicates that low-sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. Sodium 31-37 angiotensinogen Homo sapiens 86-92 28836382-11 2017 injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-sodium diet groups. Sodium 202-208 angiotensinogen Homo sapiens 13-19 28428931-5 2017 Angiotensin II is probably the most important stimulator of sodium reabsorption. Sodium 60-66 angiotensinogen Homo sapiens 0-14 27637026-1 2016 BACKGROUND: Tissue Angiotensin II (Ang-II), produced through local non ACE-dependent pathways, stimulates liver fibrogenesis, renal vasoconstriction and sodium retention. Sodium 153-159 angiotensinogen Homo sapiens 19-33 27637026-1 2016 BACKGROUND: Tissue Angiotensin II (Ang-II), produced through local non ACE-dependent pathways, stimulates liver fibrogenesis, renal vasoconstriction and sodium retention. Sodium 153-159 angiotensinogen Homo sapiens 35-41