PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20030467-8 2010 Patients with a greater potassium level elevation had a higher mean +/- SD aldosterone concentration (178 +/- 92 vs 102 +/- 57 pg/ml, p=0.007) and NR3C2 215G allele frequency (50% vs 22%, p<0.01). Potassium 24-33 nuclear receptor subfamily 3 group C member 2 Homo sapiens 147-152 20030467-11 2010 CONCLUSION: Our data suggest that potassium should be monitored with particular caution when spironolactone is started in patients with heart failure who have evidence of elevated aldosterone levels, such as high diuretic requirements, or the NR3C2 215G allele. Potassium 34-43 nuclear receptor subfamily 3 group C member 2 Homo sapiens 243-248 20583536-1 2010 Aldosterone plays an important role in blood pressure homeostasis, the regulation of circulating volume, and the maintenance of the sodium-potassium balance by binding to the mineralocorticoid receptor (MR). Potassium 139-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 175-201 20583536-1 2010 Aldosterone plays an important role in blood pressure homeostasis, the regulation of circulating volume, and the maintenance of the sodium-potassium balance by binding to the mineralocorticoid receptor (MR). Potassium 139-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 203-205 20030467-10 2010 On regression analysis, factors predictive of potassium level increases greater than 0.5 mEq/L with spironolactone were aldosterone level greater than 150 pg/ml (odds ratio [OR] 30, 95% confidence interval [CI] 3.2-287] and NR3C2 215G carrier status (OR 17, 95% CI 1.6-167). Potassium 46-55 nuclear receptor subfamily 3 group C member 2 Homo sapiens 224-229 16972228-7 2007 We demonstrate that MR mutations are extremely frequent in PHA1 patients classified according to aldosterone and potassium levels and give indications for accurate clinical and biological investigation. Potassium 113-122 nuclear receptor subfamily 3 group C member 2 Homo sapiens 20-22 16503757-6 2006 This raises the possibility that cardiac-specific antagonists of the MR may be developed that avoid the potassium retention seen with blockade of the renal MR. Potassium 104-113 nuclear receptor subfamily 3 group C member 2 Homo sapiens 69-71 15998706-10 2005 Mineralocorticoid receptor antagonism prevents the effect of activation of the renin-angiotensin-aldosterone system on PAI-1 antigen in normotensive subjects and improves fibrinolytic balance in hypertensive subjects through a potassium-independent mechanism. Potassium 227-236 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 34889107-7 2021 Elevation of the urinary potassium-to-sodium excretion ratio, reflective of mineralocorticoid receptor activity, was only observed in participants with renin-independent aldosteronism. Potassium 25-34 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-102 15212727-5 2004 In view of the potential for serious hyperkalemia with the use of aldosterone receptor blockers, it is essential to monitor serum potassium closely and to adjust the dose of aldosterone antagonists based on serum potassium levels. Potassium 130-139 nuclear receptor subfamily 3 group C member 2 Homo sapiens 66-86 15212727-5 2004 In view of the potential for serious hyperkalemia with the use of aldosterone receptor blockers, it is essential to monitor serum potassium closely and to adjust the dose of aldosterone antagonists based on serum potassium levels. Potassium 213-222 nuclear receptor subfamily 3 group C member 2 Homo sapiens 66-86 12693733-3 2003 Until further data from well-designed, prospective, randomized trials are available, the use of aldosterone receptor antagonists should be restricted to patients with severe or progressive heart failure caused by systolic left ventricular dysfunction in whom serum creatinine level is < or = 2.0 mg/dL and serum potassium levels are < 5.0 meq/L at baseline. Potassium 315-324 nuclear receptor subfamily 3 group C member 2 Homo sapiens 96-116 8191539-4 1994 The suppression of dehydrogenase activity allows glucocorticoids to activate the mineralocorticoid receptor, leading to classical mineralocorticoid type effects such as sodium retention and potassium excretion. Potassium 190-199 nuclear receptor subfamily 3 group C member 2 Homo sapiens 81-107 12015312-1 2002 Inappropriate activation of the mineralocorticoid receptor (MR) results in renal sodium retention and potassium loss in patients with liver cirrhosis. Potassium 102-111 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-58 34935140-4 2021 Canonical actions of the MR take place in epithelial cells of kidney, colon and sweat glands and contribute to sodium reabsorption, potassium secretion and extracellular volume homeostasis. Potassium 132-141 nuclear receptor subfamily 3 group C member 2 Homo sapiens 25-27 33214722-6 2021 Proper management of serum potassium is required to ensure safe clinical use of MR blockers, including awareness of at-risk patient groups, choosing appropriate dosages for therapy initiation and dosage titration, and monitoring of serum potassium during therapy. Potassium 27-36 nuclear receptor subfamily 3 group C member 2 Homo sapiens 80-82 35487592-2 2022 In recent years, it has been indicated that the MR expressed in retinal Muller cells plays an important role in regulating the potassium and water balance in the retina. Potassium 127-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 48-50 25905305-1 2000 Aldosterone promotes active sodium transport and excretion of potassium via the mineralocorticoid receptor (MR) and the resultant activation of specific amiloride-sensitive sodium channels (ENaC) and the Na-K ATP ase pump in the target tissues. Potassium 62-71 nuclear receptor subfamily 3 group C member 2 Homo sapiens 80-106 33570024-2 2021 Glycyrrhizin in licorice root activates the renal mineralocorticoid receptor increasing sodium reabsorption and potassium excretion. Potassium 112-121 nuclear receptor subfamily 3 group C member 2 Homo sapiens 50-76 25905305-1 2000 Aldosterone promotes active sodium transport and excretion of potassium via the mineralocorticoid receptor (MR) and the resultant activation of specific amiloride-sensitive sodium channels (ENaC) and the Na-K ATP ase pump in the target tissues. Potassium 62-71 nuclear receptor subfamily 3 group C member 2 Homo sapiens 108-110 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Potassium 192-201 nuclear receptor subfamily 3 group C member 2 Homo sapiens 43-69 31919958-0 2020 Cardiovascular risk associated with serum potassium in the context of mineralocorticoid receptor antagonist use in patients with heart failure and left ventricular dysfunction. Potassium 42-51 nuclear receptor subfamily 3 group C member 2 Homo sapiens 70-96 31599747-6 2020 Novel nonsteroidal mineralocorticoid receptor antagonists (MRA) are able to lower proteinuria and markers of heart failure, with limited potassium problems and without renal impairment. Potassium 137-146 nuclear receptor subfamily 3 group C member 2 Homo sapiens 19-45 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Potassium 192-201 nuclear receptor subfamily 3 group C member 2 Homo sapiens 71-73 25784710-7 2015 Overall, the use of mineralocorticoid receptor antagonists was associated with an increased serum potassium (0.23, 95% CI 0.13, 0.33 mmol/l; p<0.0001) and higher risk ratio (1.76, 95% CI 1.20, 2.57; p=0.001) of hyperkalemia. Potassium 98-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 20-46 27823598-8 2017 Patients with high potassium more often used angiotensin-converting enzyme inhibitors and mineralocorticoid receptor antagonists before admission, had impaired baseline renal function and a better diuretic response (p = 0.005), independent of mineralocorticoid receptor antagonist usage. Potassium 19-28 nuclear receptor subfamily 3 group C member 2 Homo sapiens 90-116 27823598-8 2017 Patients with high potassium more often used angiotensin-converting enzyme inhibitors and mineralocorticoid receptor antagonists before admission, had impaired baseline renal function and a better diuretic response (p = 0.005), independent of mineralocorticoid receptor antagonist usage. Potassium 19-28 nuclear receptor subfamily 3 group C member 2 Homo sapiens 243-269 26905224-10 2016 CONCLUSION: It is safe to use low dose mineralocorticoid receptor antagonists on patients receiving hemodialysis, at the end of each session of hemodialysis, and close monitoring of serum potassium levels and possible side effects is necessary. Potassium 188-197 nuclear receptor subfamily 3 group C member 2 Homo sapiens 39-65 26385038-0 2015 Facility variation and predictors of serum potassium monitoring after initiation of a mineralocorticoid receptor antagonist in patients with heart failure. Potassium 43-52 nuclear receptor subfamily 3 group C member 2 Homo sapiens 86-112 30854950-6 2018 RESULTS: Mineralocorticoid receptor antagonists result in significant improvement in blood pressure and serum potassium level among patients with primary aldosteronism. Potassium 110-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 9-35 28073850-1 2017 BACKGROUND: Heart failure guidelines recommend routine monitoring of serum potassium, and renal function in patients treated with a mineralocorticoid receptor antagonist (MRA). Potassium 75-84 nuclear receptor subfamily 3 group C member 2 Homo sapiens 132-158 25016402-9 2014 The adverse electrolyte and renal function side effects with aldosterone-receptor antagonists are not uncommon in at-risk patients, such as those with chronic kidney disease, and require that dosing be mindful of the tendency of these drugs to importantly increase serum potassium levels. Potassium 271-280 nuclear receptor subfamily 3 group C member 2 Homo sapiens 61-81 25616098-1 2015 AIM: Polymorphisms in the mineralocorticoid receptor may affect urinary sodium and potassium excretion. Potassium 83-92 nuclear receptor subfamily 3 group C member 2 Homo sapiens 26-52 23774812-7 2013 Mineralocorticoid-receptor antagonists are associated with decreased mortality in patients with heart disease and show promise in patients with kidney injury, but can elevate serum potassium concentration. Potassium 181-190 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 21799445-6 2011 For example, the number of G alleles of the N554S missense mutation (rs5527) of NR3C2 was significantly associated with greater SBP responses to potassium intervention; mean [95% confidence interval (CI)] responses (mmHg) were -3.33 (-3.65 to -3.02) for genotype A/A and -5.47 (-6.64 to -4.29) for A/G, respectively (P value = 0.0004). Potassium 145-154 nuclear receptor subfamily 3 group C member 2 Homo sapiens 80-85 27122708-1 2013 UNLABELLED: It is well-known that aldosterone plays an important role in reabsorption of sodium and fluid, and in potassium excretion in kidneys via epithelial mineralocorticoid receptor (MR) activation. Potassium 114-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 160-186 27122708-1 2013 UNLABELLED: It is well-known that aldosterone plays an important role in reabsorption of sodium and fluid, and in potassium excretion in kidneys via epithelial mineralocorticoid receptor (MR) activation. Potassium 114-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 188-190 23171954-2 2013 MR antagonists are considered to be potassium-sparing diuretics that exert their effect by blocking MR in the kidney, and they are not the first choice for treating hypertension. Potassium 36-45 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2