Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, [Sar1, Ala8]AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.
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PMID:High-output heart failure in the dog: systemic and intrarenal role of angiotensin II. 116 74

The effects of prostaglandin E1 on fluid and sodium excretion, creatinine clearance and renin release were examined in 26 hypertensive patients including 9 cases of essential hypertension, 10 of renovascular hypertension and 7 of primary aldosteronism. When prostaglandin was infused intravenously in a total dose of 120 mug in 60 min, urine volume was increased in 70% of cases, and sodium excretion in 61%, but little changes were observed in creatinine clearance. The most prominent diuresis and natriuresis were obtained in primary aldosteronism (mean increase was 319% in urinary volume, and 222% in sodium output). The average increases in urinary volume were 61% in patients with essential hypertension and 97% in renovascular hypertension. And urinary output of sodium was increased by 63% in the former and 56% in the latter. The remarkable renal effects of prostaglandin E1 in primary aldosteronism were completely abolished after the administration of spironolactone. Significant elevation of plasma renin activity resulted from prostaglandin E1 infusion in essential hypertension, while no constant effect was obtained in renovascular hypertension and primary aldosteronism. The present experiments indicate that prostaglandin E1 has different effects on the kidney according to the types of hypertension and the effects correlate closely with patient's status of extracellular fluid volume or sodium balance.
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PMID:Renal effects of prostaglandin E1 in hypertensive patients. 118 18

From 1966 to 1975, 38 patients underwent 42 procedures for renovascular hypertension; 35 operations were aortorenal bypasses and 7 were nephrectomies. Forty-five per cent of the patients were cured, 43% were improved and 12% were unimproved. There were no operative deaths and only three late deaths. Two grafts occluded and 2 became stenotic, giving a graft complication rate of 12%. Curability was best correlated with a short history of hypertension and a pathologic diagnosis of fibromuscular hyperplasia, but not with patient age. Most patients selected for surgery had elevated renal venous renin ratios, and of these 95% were cured or improved. Of those with normal renin ratios, 85% were still cured or improved. Postoperative aortography and peripheral renin measurements offered valuable information in predicting the ultimate response to surgery. Preservation of renal function was a principal indication for surgery in 11 patients. In 8, azotemia was documented preoperatively. Hypertension was cured or improved in every case and 5 patients demonstrated a 10-50% reduction in BUN and creatinine following revascularization.
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PMID:Operative management of renovascular hypertension. 119 Aug 80

Potassium canrenoate was administered intravenously, twice at a 9-hr interval, to 3 apparently healthy male volunteers. No consistent changes in endogenous creatinine or PAH clearances were observed for 6 hr after the initial 200-mg dose of this aldosterone antagonist. The clearance of canrenone (the major gamma-lactone metabolite) exceeded by 70% the simultaneous clearance of creatinine from the second through the sixth hour. The excretion of canrenone amounted to 6.8 mg (3.4%) of the dose during the 6-hr clearance study, but was nearly absent (0.2 mg) during the ensuing 6- to 9-hr period. The cumulative excretion of the glucuronide conjugate of canrenone amounted to 4.6 and 2.8 mg (2.3% and 1.4%) of the dose during these respective periods. A sustained retention of K was observed in 1 subject. Otherwise, as was anticipated in the absence of hyperaldosteronism, urinary electrolyte levels were essentially unchanged. Circulating aldosterone and plasma renin activity levels were essentially unaltered.
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PMID:Renal clearance of canrenoate in normal man. 120 80

Based on repeat measurements in 11 male and 12 female normal subjects, aged 20 to 35 years, on normal, low and high sodium intake a nomogram for the relation between fasting urinary sodium creatinine ratio and plasma renin activity (PRA) is presented. The use of fasting urinary sodium creatinine ratio as index of sodium intake and hydration of the subject results in a better prediction of PRA as compared with 24-hour urinary sodium excretion. Although fasting urinary sodium creatinine ratio in normal subjects on a normal sodium intake varies between 0.2 and 1.6, a uniform increase of basal PRA is found only at a ratio of below 0.3. A ratio greater than 0.5 excludes any stimulation of PRA by low sodium intake and (or) dehydration of the subject. The shape of the nomogram should make it applicable independent of the method used for PRA assay, as soon as the variation of PRA in normal subjects with a urinary sodium creatinine ratio above 0.5 is established.
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PMID:[Nomogram for the relation between plasma renin activity and fasting urinary sodium creatinine ratio (author's transl)]. 120 1

The renin-angotensin system was studied in rats suffering from hereditary hydronephrosis in which normal blood pressure, hyperkalemia, and damage to the renal medulla and distal tubules were found. An increased serum creatinine level, decreased creatinine clearance and increased 24 hrs urine volume were observed in rats with bilateral hydronephrosis. When compared to rats with normal kidneys, bilaterally hydronephrotic animals exhibited elevated plasma renin activity (9.9 +/- 1.3/S.E./ng AI/ml/hr vs. 2.4 +/- 0.4 in rats with normal kidneys), and decreased renal renin concentration (78 +/- 4 mug AII/g vs. 132 +/- 5). No correlation between the extent of kidney damage and renal renic concentration was found. After the hyperkalemia of the hydronephrotic rats was corrected, there were significant increases in both plasma renin activity and renal renin concentration, but the renal renin concentration remained significantly lower than that observed in animals with normal kidneys. The results suggest that renin production and/or storage capacity are diminished in hydronephrotic kidneys.
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PMID:The renin-angiotensin system in rats with hereditary hydronephrosis. 123 6

We have assessed the capacity of an analogue of angiotensin II (A II), 1-Sar, 8-Ala A II (P113) in normal man to stimulate and block responses to A II in four systems: blood pressure was monitored directly from an arterial catheter, and renal blood flow was measured with 133Xe and arterial renin and aldosterone concentrations by radioimmunoassay. The 31 normal subjects were in balance on a daily intake of 200 meg sodium and 100 meq potassium to suppress endogenous renin. P113 administered intravenously induced a dose-related renal blood flow reduction, with a threshold dose of 0.1 mug/kg/min. This dose also induced a small but significant increase in arterial blood pressure and plasma aldosterone as well as a reduction in plasma renin activity. In contrast to its effect on the renal vasculature, no tendency to a progressive response in the latter three parameters was noted as the P113 dose was increased 30-fold, to 3.0 mug/kg/min. P113 also reduced the clearance of para-aminohippurate, creatinine, sodium, and potassium, a pattern similar to that induced by A II. P113 at 0.1 mug/kg/min reduced significantly the blood pressure and renal vascular and aldosterone responses to graded doses of A II. Higher P113 doses totally obliterated all three responses to A II infused at 10 ng/kg/min, a dose that provides arterial A II concentrations in the range found in angiotensin-mediated hypertension. When A II was infused first, to induce a pressor, renal vascular, and aldosterone response, P113 induced a dose-related reversal of the response in each system. In conclusion, P113 is a partial agonist in normal man, inducing an angiotensin-like response in settings in which endogenous A II is not playing a tonic role, and displaying dominant antagonist activity in settings in which A II is active. Moreover, the studies suggest that the receptors mediating the responses to A II are different in the renal vasculature and other systemic vascular beds. The adrenal receptor must also differ. This agent should be useful in dissecting the role of A II in diseases characterized by hypertension or abnormalities of renal and adrenal function.
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PMID:Blockade and stimulation of renal, adrenal, and vascular angiotensin II receptors with 1-Sar, 8-Ala angiotensin II in normal man. 124 2

The excretion of creatinine, VMA, and aldosterone was measured in the urine of 14 normal and 25 persons with stable essential hypertension during a day time (7.00-23.00 hrs) and a night time (23.00-7.00 hrs) period. Excretion of VMA and aldosterone per hour in the two groups was lower during the night period than during the day. No significant difference existed between the excretion values of both groups. Night/day rations for the excretion of VMA and of aldosterone respectively, per mg of creatinine excreted were calculated for each subject. In the normal group the night/day ratios of aldosterone excretion showed a significant correlation to the corresponding ratios of VMA excretion; such correlation was not found in the hypertensive group. The fact that a correlation was observed in the normal group is compatible with the hypothesis that catecholamines are involved in the regulation of the renin-angiotensin-aldosterone system. Lack of correlation in the group of hypertensive does not as yet allow any conclusions. In two patients with primary hyperaldosteronism, the aldosterone excretion during the night was relatively more elevated than in the day.
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PMID:[Diurnal variation in the urinary excretion of vanilmandelic acid and aldosterone in normal and hypertensive persons (author's transl)]. 125

The protease inhibitor aprotinin was given a) in experimental septic shock, and b) in patients with hepatic cirrhosis and ascites, since in both conditions, activation of the plasma kallikrein-kinin system is associated with pathological systemic vasodilatation, which may trigger reflex neuroendocrine activation and renal solute retention. Given early in experimental sepsis, aprotinin maintained the arterial pressure, systemic vascular resistance (SVR), creatinine clearance and sodium excretion, all of which fell in controls. Aprotinin also blocked increases in pulmonary artery pressure and plasma renin activity (PRA). Given late in sepsis, aprotinin caused a rapid rise in arterial pressure and SVR towards baseline levels. In cirrhosis, aprotinin increased SVR in patients with low baseline values, and improved glomerular filtration rate, renal plasma flow and sodium excretion in all subjects; PRA was suppressed by aprotinin. Aprotinin reverses pathological systemic vasodilatation in these two conditions, and this is associated with a reduction in renin release and improved renal function.
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PMID:Vasoactive effects of aprotinin. 128 72

The pharmacokinetics and pharmacodynamics of nilvadipine, a new dihydropyridine calcium antagonist, were examined in 16 patients divided into two different population groups. The first group of eight patients had arterial hypertension with limited renal function (creatinine clearance of 15-50 ml/min). The second group of eight patients had arterial hypertension with no concomitant renal dysfunction (creatinine clearance over 80 ml/min). Following a 1-week placebo washout period, all patients were given 8 mg of nilvadipine once daily for 10 days. The diastolic blood pressure (24-h postdose) fell in group I from a mean of 100.5 to 91.5 mm Hg and in group II from a mean of 106.7 to 88.2 mm Hg, which was significant in comparison to the placebo period. In neither group was there a significant change in heart rate, renin and aldosterone plasma levels, serum electrolytes, or sodium and potassium excretion. The pharmacokinetics of the unchanged nilvadipine were not significantly different between group I and group II. Neither group showed unchanged nilvadipine in urine. There was a slight increase in plasma levels of the inactive main metabolites M3 and M7; there was correspondingly less M3 found in the urine of group I patients. Nilvadipine appears to be an effective hypotensive agent at single daily doses of 8 mg. This dosage was well tolerated. The findings of this study did not suggest that lower doses need to be given to patients with limited renal function, at least not those with a creatinine clearance between 15 and 50 ml/min.
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PMID:Nilvadipine in hypertension with renal dysfunction. 128 94


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