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)

Eleven patients with hypertension secondary to renal disease were treated with hydrochlorothiazide or furosemide plus other drugs to normalize blood pressure. Creatinine clearance fell during the initial treatment period, but then either remained constant or rose toward pretreatment levels in spite of continued therapy. Plasma renin activity was low-normal to subnormal in eight of the 11 patients prior to therapy and did not rise significantly with therapy. Aldosterone excretion was within the normal range prior to treatment and remained normal or increased moderately with treatment. This study demonstrates that diuretics effectively reduce blood pressure in patients with hypertension secondary to renal disease without producing severe volume depletion or clinically significant reduction in renal function. The low renin levels are consistent with other evidence that hypertension in these patients is related to salt and water retention.
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PMID:Use of diuretics in treatment of hypertension secondary to renal disease. 70 75

Plasma renin activity (PRA) was measured during the administration of clonidine (0.1 mg twice daily) to 11 patients with essential hypertension. After eigth weeks a trend toward an increase in PRA was noted. This increase was significant in "low renin" subjects (less than 1 ng Al/ml/hr, n = 7) in whom PRA (ng/ml/hr +/- SEM) rose from a control value of 0.7 +/- 0.1 to 2.0 +/- 1.1 at one week, 5.6 +/- 2.1 at four weeks, and 4.4 +/- 1.0 at eight weeks (p less than 0.05). In contrast, in a small group of "normal renin" patients (n = 4), PRA did not change significantly but tended to decrease on clonidine therapy from 9.2 +/- 3.4 at control to 3.3 +/- 2.0 at one week, 3.4 +/- 0.6 at four weeks, and 4.7 +/- 1.7 ng Al/ml/hr at eight weeks. Plasma renin substrate and serum and urinary electrolytes did not change significantly in either group and blood pressure reduction was comparable in the two groups. A strong negative correlation (r = -0.84, p less than 0.001) was found between changes in creatinine clearance and changes in PRA. Previous studies have implicated alpha-adrenergic receptors as the site of clonidine actions on blood pressure and renin release. The observed renin stimulation during chronic administration of clonidine to "low renin" patients with essential hypertension may imply an altered intrarenal alpha-receptor function in "low renin" essential hypertension.
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PMID:Renin stimulation during clonidine therapy in "low renin" essential hypertension. 72 16

The effect of papaverine on renal function and renin release was investigated in dogs in vivo and in vitro. Intrarenal arterial infusion of 0.1 mg/kg/min of papaverine for 10 minutes caused a significant rise in renal blood flow, a significant decrease in renal vascular resistance, clearance and extraction ratio of creatinine and PAH and in the amount of filtered sodium, without altering arterial blood pressure. There was a significant increase in sodium excretion and in the excreted percentage of filtered sodium (TRFNa). Renin activity (PRA) of arterial blood and renal venous blood, veno-arterious PRA-difference and renin secretion increased significantly after papaverine infusion. In order to eliminate the effect of hemodynamic changes on renin secretion, the effect of papaverine (10(-5), 10(-4)M) was investigated in vitro in surviving canine kidney cortex slices. Papaverine caused a significant increase in renin release and in tissue cAMP concentration. This supports the assumption that the increase in renin secretion might be due to a direct effect on the juxtaglomerular apparatus, by blocking phosphodiesterase activity and by increasing the renal cAMP level.
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PMID:Effect of papaverine on renin release in dogs in vivo and in vitro. 75 46

In 10 healthy and 27 diabetic children aged 11--17 years plasma renin activity was determined in horizontal position (PRA-I) and after stimulation by furosemid and upright position (PRA-II). In diabetic children with or without hypertension and protein-uria, and a normal or only slightly elevated plasma creatinine level normal PRA-I and PRA-II values were found.
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PMID:[Plasma renin activity in diabetic children (author's transl)]. 76 47

Vascular responsiveness to infused angiotensin II and to norepinephrine was determined in 14 normal subjects and two groups of diabetic subjects, 16 with no clinically detectable diabetic complications and 14 with diabetic retinopathy but no clinical evidence of nephropathy. All were maintained on a 100-mEq. -Na- 100-mEq. -K diet. Serum electrolytes, 24-hour urinary sodium, creatinine clearance, and plasma renin activity did not differ significantly among the groups. Group mean baseline diastolic pressure in those with retinopathy was higher than in normal subjects but no significantly different from that of uncomplicated diabetics. The pressor dose of angiotensin II (ng./kg./min. to increase diastolic blood pressure 20 mm. Hg) for each group respectively was 11.5 +/-0.9, 12.9+/- 1.3, and 8.3 +/- 1.3, and the slope of the dose-response curve (mm. Hg rise in blood pressure resulting from the infusion of 1 ng./kg./min. following the initial increment in blood pressure) was 2.0 +/-0.2, 1.6+/-0.2, 3.3+/- 0.6. For norepinephrine, the pressor doses were 163 +/- 24, 212+/-21, and123 +/- 11 and slopes were 0.17 +/- 0.03, 0.13 +/- 0.02, and 0.20 +/-0.02. Neither diabetic group differed significantly from normal subjects. Diabetics with retinopathy were more sensitive to angiotensin II, pressor dose (P less than 0.059) and slope (P less than 0.02), and to norepinephrine, pressor dose (P less than 0.006) and slope (P =0.05) than those without complications. These data suggest that vascular reactivity is enhanced in diabetics with retinopathy.
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PMID:Vascular reactivity to angiotensin II and to norepinephrine in diabetic subjects. 77 23

Thirteen acutely symptomatic malignant hypertensive patients were treated with minoxidil in combination with a beta-adrenergic blocking agent and diuretics or dialysis. The degree of endorgan involvement varied, with the kidney being the most compromised in 11 of 13 patients. In 12 of 13 patients, MABP (mean arterial blood pressure) fell significantly within 72 hours, P less than 0.005. After 20 months of therapy, all have now had a favorable response, with a mean reduction in MABP of 48 mm Hg, and with no adverse cardiac disturbances. In addition, the patients with mild azotemia had an improvement in renal function as determined by a reduction in serum creatinine. PRA (peripheral renin activity) rose with the addition of minoxidil despite therapeutic concentration of serum propranolol and a reduction in MABP and heart rate. It was also noted that those patients who had been on guanethidine prior to minoxidil had a more pronounced lowering of MABP within 72 hours of minoxidil therapy. It is concluded that minoxidil is a safe, fast, and effective agent to achieve rapid and sustained control of MABP in malignant hypertensive states associated with chronic renal insufficiency.
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PMID:Long-term effects of minoxidil in the treatment of malignant hypertension in chronic renal failure. 78 12

1. Patients with cadaveric renal transplants and plasma creatinine less than 177 micronmol/l who had their own kidneys removed were studied. 2. The renin-angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. 3. The renin-angiotensin system had no major role in the establishment or maintenance of hypertension. 4. Mean arterial pressure was directly related to expansion of the extracellular fluid volume.
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PMID:Plasma renin activity, plasma angiotensin II and extracellular fluid volume in patients after renal transplantation. 79 52

Urinary prostaglandins E2 and F2alpha were measured by gas chromatography-mass spectrometry in three adult women and an adolescent girl with Bartter's syndrome. On a constant metabolic diet prostaglandin E2 ranged from 293 to 1,221 ng/day (mean, 640 ng/day) and exceeded the normal range for adults of 76 to 281 ng/day in all patients. Prostaglandins F2alpha ranged from 291 to 1,061 ng/day (mean, 747 ng/day) in the adult women. Only in a young girl did prostaglandins F2alpha (1,677 ng/day) clearly exceed the normal range for adults of 422 to 871 ng/day. Treatment with indomethacin, which decreased urinary prostaglandin E-like material by 69 per cent or more, did not affect blood pressure. Plasma renin activity, which ranged from 5.2 to 22.2 ng/ml/hour (patients supine) and from 23.3 to 30.4 ng/ml/hour (patients upright), and urinary aldosterone, which ranged from 14.0 to 45.6 ng/day, decreased by 79, 65 and 52 per cent, respectively. The clearance of creatinine was lower for the eight or nine days of treatment, the balances of sodium and potassium were positive, and serum potassium was higher than in control. Ibuprofen, an inhibitor of prostaglandin synthetase which differs in structure from indomethacin, produced metabolic effects which were qualitatively similar to those of indomethacin. The results indicate that the renal synthesis of prostaglandins is increased in Bartter's syndrome and that prostaglandins mediate the hyperreninemia and hyperaldosteronism which characterize the disorder. The over-production of prostaglandins by the kidney could be proximal cause of the syndrome, or secondary to intrarenal changes of an unknown nature. This study provides additional evidence for an important role for prostaglandins in the release of renin.
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PMID:Bartter's syndrome: a disorder characterized by high urinary prostaglandins and a dependence of hyperreninemia on prostaglandin synthesis. 82 Jan 94

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension. 83 Apr 37

We have previously reported that infusion of CaCl2 into the renal artery of the dog inhibits renin release. To evaluate the possible importance of the anion delivered with calcium, similar experiments were performed in 10 dogs with equivalent amounts of calcium gluconate (0.3 mg. of Ca++ per kilogram of body weight per minute). The experiment consisted of three successive 15 minute control periods, followed by three 15 minute calcium gluconate infusion periods and two 15 minute recovery periods. During calcium gluconate infusion, mean serum Ca++, and ECa++, ENa+, and EFNa+ from the infuses kidney increased (p less than 0.005). Systolic blood pressure (142 mm. Hg +/- 8S.E.), renal blood flow (137 ml. per minute +/- 11 S.E.), creatinine clearance, and aldosterone excretion (12.0 ng. per 15 minute +/- 1.5 S.E.) did not change (p less than 0.3). Renal venous PRA (28.4 ng. per millileter per hour +/- 7.5 S.E.) decreased (p less than 0.014). The per cent decrease of PRA correlated (r = -0.70) with the per cent increase EFNa+ (p less than 0.001). Calcium gluconate had a lesser (p less than 0.01) inhibitory effect on renin than CaCl2, despite greater excretion of Ca++ and Na++ during calcium gluconate infusion. Taken together, the results indicate that Ca++ inhibits renin release, although the extent of the inhibition is modified by the anion accompanying Ca++. The effect of Ca++ on renin may be mediated by NaCl transport across the macula densa.
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PMID:Effect of calcium gluconate infusion on renin in the dog. 83 Jul 78


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