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)

Changes in blood pressure, heart rate, electrolyte excretion, and the renin-angiotensin-aldosterone system were monitored before and after minoxidil was added to a regimen of a diuretic and propranolol hydrochloride in 12 severely hypertensive patients. None required more than 40 mg of minoxidil daily for control. On a constant intake, urinary sodium excretion decreased, while urinary potassium excretion remained stable. Heart rate, body weight, and plasma volume increased, while creatinine clearance did not change. Although plasma renin activity increased fourfold, the plasma aldosterone concentration did not increase. Six subjects were restudied after two months of minoxidil treatment. Although blood pressure control continued to be excellent in these subjects, plasma renin values and plasma volume had returned to pretreatment levels. These studies suggest that minoxidil rapidly and effectively lowers blood pressure. Although sodium retention accompanies minoxidil administration acutely, the effect is independent of aldosterone and may be transient.
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PMID:Rapid blood pressure control with minoxidil: acute and chronic effects on blood pressure, sodium excretion, and the renin-aldosterone system. 44 47

To study the influence of arterial pulse pressure on renin release, a chronic pulseless calf preparation was developed using a centrifugal left ventricular bypass blood pump. After pump implantation and recovery, control measurements of renal vein and arterial plasma renin activity, arterial pressure, and renal artery flow were obtained. The centrifugal bypass pump rate then was increased to capture cardiac output completely, and nine conscious calves were perfused in a nonpulsatile manner (pulse pressure less than 5-10 mm Hg) for 48 hours. Nonpulsatile perfusion was well tolerated and serum sodium, potassium, creatinine, and blood urea nitrogen were unchanged during bypass. Mean arterial pressure remained relatively constant [114 +/- 3 (SE) mm Hg] during bypass, and was not significantly changed from control. Although renal blood flow decreased slightly from control (667 +/- 84 ml/min) during the nonpulsatile perfusion period (555 +/- 73 ml/min), renin secretion did not increase significantly from control (482 +/- 81 ng angiotensin I/ml per hr per min) during the bypass period (531 +/- 99). A diurnal cycle of renin secretin was observed during the pulseless perfusions. These data document the lack of any significant stimulatory influence of decreased pulse pressure on renin secretion in a chronic awake calf model.
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PMID:Renin secretion in the chronically perfused pulseless calf. Evidence for failure of stimulation by decreased pulse pressure. 44 91

Renal function is known to be abnormal in patients with cirrhosis. Diminished cortical blood flow due to active renal vasoconstriction is present. Renal prostaglandins, potent vasodilators, could be released by the kidney in an attempt to maintain renal blood flow. This possibility was investigated by measuring the effect of indomethacin, an inhibitor of prostaglandin synthetase, in patients with alcoholic liver disease. Administration of indomethacin reduced the effective renal plasma flow (ERPF) and creatinine clearance by 23% and 19%, respectively (P less than 0.001), and increased serum creatinine by 29% (P less than 0.001). The response to indomethacin was variable (fall in ERPF (+)7.8% to (-)67%), but was greatest in patients with ascites. Eighty percent of ascitic patients had a greater than 15% fall in ERPF after administration of indomethacin compared with 20% of nonascitic patients (P less than 0.025). An infusion of prostaglandin A1 in 13 patients corrected the decrease in ERPF and creatinine clearance that had followed the administration of indomethacin. The administration of indomethacin caused a significant fall in plasma renin activity, 8.2 +/- 2.5 to 3.6 +/- 1.4 ng/ml/hr (P less than 0.025). The fall in plasma renin activity occurred when ERPF was depressed maximally, suggesting that endogenous prostaglandins exert more control over renin release than does ERPF. Prostaglandins appear to be an important factor in maintaining renal blood flow in patients with cirrhosis and sodium retention.
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PMID:Effect of indomethacin and prostaglandin A1 on renal function and plasma renin activity in alcoholic liver disease. 44 34

Fifteen patients with chronic liver disease having a peritoneovenous shunt for chronic intractable ascites were studied prospectively for renal function and hemodynamic changes during balance studies, pre-, peri-, and postoperatively. Shunt insertion caused a rapid redistribution of ascites into the intravascular compartment with hemodilution and significant rises in cardiac output (9 patients) (P less than 0.025) renal blood flow (3 patients) (P less than 0.025), and creatinine clearance (15 patients) (P less than 0.005), and decreases in plasma renin activity (10 patients) and serum aldosterone levels (9 patients) (P less than 0.025). Despite these changes, small repeated doses of furosemide were required to start and maintain a diuresis and natriuresis with sodium excretion rising from 7.2 +/- 4.1 to 174 +/- 44 meq/day (P less than 0.0005) in the 15 patients. At 2 wk postoperatively, the 15 patients had lost a mean of 7.5 kg in weight associated with a persistent improvement in creatinine clearance and a continued natriuresis, 15.9 +/- 7 mEq/day (P less than 0.005), despite no statistically significant change in cardiac output (7 patients) or renal blood flow (4 patients) compared with preoperative levels. This operation is an effective therapy for refractive ascites, but the incidence of potentially fatal complications makes us hesitate to recommend it except for patients resistant to normal conservative measures.
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PMID:The renal and hemodynamic effects of the peritoneovenous shunt for intractable hepatic ascites. 44 39

Prostaglandins may modulate renal function and play a role in the hyperreninism and angiotensin pressor resistance of chronic liver disease. To study this possibility, we evaluated 12 patients with alcoholic cirrhosis and ascites. Urine immunoassayable prostaglandin E in 5 female patients was 3.3 +/- 0.5 micrograms/day [normal, 0.3 +/- 0.1 (SE)], renin was 14.6 +/- 3.7 ng/ml.h, and aldosterone was 76 +/- 19 ng/dl. After either indomethacin (200 mg) or ibuprofen (2000 mg) for 1 day, urine immunoassayable prostaglandin E fell to 0.8 +/- 0.4 micrograms/day, renin to 8.0 +/- 2.4 ng/mol.h, and aldosterone to 54 +/- 14 ng/dl (all P less than 0.01). Pressor sensitivity increased dramatically, and creatinine clearance transiently fell from 73 +/- 10 to 32 +/- 7 cc/min (P less than 0.01). Because a primary effect on renin might explain the renal impairment, an additional study used propranolol to lower renin activity. Renal function was unaltered by propranolol. We conclude that prostaglandins play a supportive role in maintaining renal function and are involved in the hyperreninism and pressor resistance of patients with liver disease.
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PMID:Prostaglandins: modulators of renal function and pressor resistance in chronic liver disease. 44 95

Plasma renin activity has been measured daily in 36 patients suffering from self poisoning with acetaminophen. In 3 developing porto-systemic encephalopathy terminal renal failure developed with high plasma renin activity. In 2 who developed acute renal failure without porto-systemic encephalopathy, plasma renin activity was noted to rise before serum creatinine and to return to initial levels after 3 or 4 days while renal failure persisted. Six other patients with similar hepatic damage showed comparable rises in renin without developing renal failure. Our findings are consistent with but do not establish a pathogenetic role for renin in acetaminophen-induced acute renal failure. It is suggested that other factors may act with renin to bring about renal failure.
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PMID:Plasma renin activity during the development of paracetamol (acetaminophen) induced acute renal failure in man. 45 18

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

A case is presented of a 1-year-old boy with hypertension resulting from abnormal renin production by the right kidney. The kidney had undergone infarction and atrophy secondary to renal vein thrombosis. The left kidney remained normal despite inferior vena cava thrombosis because of the development of collateral venous circulation. The hypertension was cured by right nephrectomy. The child remains normotensive and with a normal serum creatinine at 1-year followup.
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PMID:Hypertension in childhood from renal vein thrombosis. 47 18

Plasma renin activity was determined in 25 healthy, full-term, newborn infants aged 1 day to 9 weeks. High values were found, the mean level at 1-2 days of life (24.8 +/- 8.4 ng/ml/hr, SE) being significantly higher than the mean levels at 7-9 days (5.8 +/- 1.5) and at 4-9 weeks (8.1 +/- 1.3) (P less than 0.05). No correlation was found between plasma renin activity and systolic blood pressure, hematocrit, creatinine clearance, serum sodium, or serum potassium. Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). The correlations reached higher coefficients if only infants aged less than or equal to 9 days were considered. In addition, vasopressin was measured by radioimmunoassay in the urine. The daily excretion was lower in newborn infants (9.4 +/- 1.6 ng/m2/day, SE, at 1-2 days of postnatal life) than in healthy children (37.1 +/- 5.6), and was significantly correlated with creatinine clearance (r = 0.69), but not with urinary osmolality.
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PMID:Plasma renin activity related to sodium balance, renal function and urinary vasopressin in the newborn infant. 48 42

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.
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PMID:Hypertension and hyperkalaemia responding to bendrofluazide. 50 50


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