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)

Basically, the determination of the plasma renin activity (PRA) consists of the in vitro generation of angiotensin I and the radioimmunological determination of angiotensin I. Since both steps can be performed in several ways, the results from different laboratories can hardly be compared. In this paper we have described the results of our attempts to standardize both steps of the PRA determination currently in use in our laboratory, against Research Standard A for Angiotensin I and the International Reference Preparation of Human Renin, both obtained from the Medical Research Council.
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PMID:On standardizing the determination of the plasma renin activity. 63 20

Urinary renin activity (URA) was measured by radioimmunoassay in sequential studies of 5 patients with acute renal failure (ARF) and in 13 normal volunteers. URA was elevated during the oliguric phase of ARF and fell to low levels prior to resolution of oliguria. Plasma renin activity (PRA) varied approximately in response to changes in intravascular volume status. In normal volunteers, the very low URA values did not change following furosemide-induced increases in PRA. A simple, rapid, and accurate method is described for the measurement of URA in humans by radioimmunoassay of angiotensin I generated during incubation of urine with homologous plasma substrate. The urinary enzyme exhibited the same properties as purified human renal renin and the incubation product appeared identical to angiotensin I standard. Renin activity in urine was directly proportional to enzyme concentration and no evidence was obtained for interference from other proteolytic activities or from inhibitors or promoters of renin in urine.
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PMID:Measurement of urinary renin activity by radioimmunoassay: sequential studies in acute renal failure in man. 64 43

1. Intravenous infusion of the individual components of the renin-angiotensin system caused drinking in dogs in water balance. 2. Angiotensin II was the most potent and rapidly acting peptide inducing drinking. The minimum effective rate of infusion was between 8.3 and 16.6 X 10(-12) mole kg-1 min-1 which yield blood levels of angiotensin II that fell well within physiological limits for the dog and were mildly pressor. Angiotensin I and synthetic renin substrate caused less drinking than angiotensin II, and angiotensin III was the least effective dipsogen. 3. Renin caused significant drinking when infused I.V. at a rate of 0.5 u. min-1 for 15 min. Drinking was slower in onset and continued for longer than after other components of the renin-angiotensin system. 4. Within the dose range 1875-15,000 X 10(-12) mole of angiotensin II the amount of water drunk depended more on the rate of infusion than on the duration of the infusion. 5. During an I.V. infusion of angiotensin II lasting 2 hr, the rate of drinking was greatest during the first 15 min. After this declined progressively. 6. A delay of 1 hr after the start of an intravenous infusion of angiotensin II before access to water was allowed, did not significantly reduce the amount of water drunk. Nor did infusion of isotonic saline for 105 min reduce drinking in response to a subsequent infusion of angiotensin II. However, a preload of dilute milk approximately equal in volume to the amount of water normally drunk in response to I.V. angiotensin II significantly reduced drinking. Therefore the dog stopped drinking during long-term infusions of angiotensin II owing to the action of satiety mechanisms and not to tachyphylaxis or fatigue. 7. Intracarotid infusion of angiotensin II, angiotensin I, synthetic renin substrate and angiotensin III, at 40 X 10(-12) mole min-1 also caused drinking. Intakes of water were similar to the intakes after I.V. infusion at six times the arterial rate, except that angiotensin I was relatively less effective by intracarotid infusion than by I.V. infusion. 8. Renin, infused at 0.5 u. min-1 for 15 min, was much less effective by intracarotid infusion than by intravenous. 9. These results are compatible with a role for circulating angiotensin II in the thirst of hypovolaemia or moderate extracellular dehydration.
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PMID:Systemic angiotensin-induced drinking in the dog: a physiological phenomenon. 65 Apr 70

Human renal renin (EC 3.4.99.19) and pseudorenin were easily separated in a single step by affinity chromatography on hemoglobin-Sepharose-2B. Renin and pseudorenin were monitored by their actions on crude and partially purified hog protein renin substrates at neutral and acidic pH and on synthetic labelled polymeric renin substrate. Under the conditions employed (0.1 M sodium acetate (pH 3.5)/1 M sodium chloride at 4 degrees C) renin does not bind to the affinity adsorbent while pseudorenin is effectively bound and can be eluted only after raising the pH to 6.5. Pseudorenin-free renin prepared by this method is devoid of proteolytic activity toward hemoglobin. The chromatographic behaviour of renal pseudorenin on hemoglobin-Sepharose-2B is similar to that of cathepsin D.
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PMID:Separation of human renal renin and pseudorenin by affinity chromatography on hemoglobin-Sepharose-2B. 65 43

The effects of ouabain or ouabain and furosemide on renal function and renin secretion were studied in conscious isovolemic sheep. The sheep received a continuous renal arterial infusion of papaverine, 7 mg/min, throughout the experiment. Ouabain alone (7 X 10(-7) M in the renal plasma) produced significant decreases in glomerular filtration rate (GFR) and renal plasma flow (RPF) but not in renal perfusion pressure. Plasma [K+] rose after ouabain administration. Fractional (FENa) and absolute (UNaV) Na+ excretion were 2.9 +/- 1.0% (mean +/- SE) and 78 +/- 54 muEq/min, respectively, during the papaverine infusion and rose to 19 +/- 5.1% (P less than 0.05) and 528 +/- 116 muEq/min (P less than 0.01) after ouabain administration. Despite the large changes in Na+ reabsorption, renin secretion was not stimulated. During the control period, renin secretion was 281 +/- 131 ng/min and the average renin secretion after ouabain administration was 310 +/- 78 ng/min (not significant). A smaller dose of ouabain (2 X 10(-7) M) infused into the renal artery with 40 mg of furosemide, iv, did not decrease GFR but RPF was suppressed. FENa and UNaV averaged 4.4 +/- 1.6% and 121 +/- 44 muEq/min, respectively, while papaverine was infused into the renal artery and increased to 18 +/- 4.8% (P less than 0.05) and 636 +/- 209 muEq/min (P less than 0.05) after ouabain and furosemide were infused. Renin secretion was 118 +/- 62 ng/min during the control period and averaged 240 +/- 67 ng/min after ouabain plus furosemide. The difference was not statistically significant. Thus ouabain alone does not stimulate renin secretion in the conscious, isovolemic sheep despite a presumed increase in [NaCl] at the macula densa and inhibition of NaCl transport by the loop of Henle. Ouabain also blocks the normal stimulatory effects of furosemide on renin secretion.
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PMID:Renal function and renin secretion after administration of ouabain and ouabain plus furosemide in conscious sheep. 65 58

Renin concentration was determined in plasma and amniotic fluid samples immediately after collection, after storage at -18 degrees C for up to 48 h, and after storage at 5 degrees C for as long as 48 h. Renin concentration increased, both in plasma (p less than 0.05) and amniotic fluid (P less than 0.02), after the storage at 5 degrees C, but no significant alteration occurred on storage at -18 degrees C. Partial activation of inactive renin could explain the observed increase in renin concentration at 5 degrees C.
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PMID:Increased renin concentration in plasma and amniotic fluid during storage. 65 82

To learn more about the regulation of blood pressure in renal parenchymal disease, 57 subjects (18 normal controls, 25 patients with essential hypertension and 14 with renal parenchymal disease and hypertension) were evaluated for peripheral renin activity, 24-hour urinary kallikrein activity and whole-blood volume. Blood volumes were significantly lower in patients with essential hypertension (P less than 0.001) and those with renal disease and hypertension (P less than 0.001) than in normotensive subjects. Renin activities (measured after the subjects were standing) were also lower in patients with essential hypertension and hypertension due to renal disease (P less than 0.01 and P less than 0.02, respectively). Kallikrein activity was similar in subjects with renal disease and those with hypertension (P less than 0.05) but markedly diminished in both groups as compared with normotensive subjects (P less than 0.001 and P less than 0.01, respectively) when glomerular filtration rates were taken into account. The kallikrein-kinin system may be involved in the hypertension associated with renal parenchymal disease.
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PMID:Urinary kallikrein activity in the hypertension of renal parenchymal disease. 66 89

Twelve patients with cirrhosis, refractory ascites, and varying degrees of renal failure (creatinine clearance, 5 to 44 ml/min) were studied before and up to 2 weeks following peritoneovenous shunt. Creatinine clearance increased 60% or more in seven patients (group I) and 22% or less in five patients (group II). There were no significant differences in maximum urine output or sodium excretion between groups (group I, 4,272 ml/14 hr, 372 mEq/24 hr; group II, 3,722 ml/24 hr, 255 mEq/24 hr). Aldosterone and renin concentrations were higher in group I and showed a greater decrease after shunting. Renin substrate levels also were higher in group I and rose following shunt insertion, while group II remained low. Ascitic fluid was found to contain renin substrate in concentrations of approximately 25% to 50% of plasma concentrations. Patients with the greatest increase in creatinine clearance showed the largest rise in substrate concentration and fall in renin and aldosterone secretion, suggesting a dynamic relationship between these factors. That a diuresis could occur without significant change in these parameters in five of 12 patients suggests independent control mechanisms for renal salt and water excretion and glomerular filtration in the ascitic patient.
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PMID:Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. 66 20

1. Renin release from isolated dog renin granules was limited to within 20% of the total renin during incubation at 37 degrees C in isotonic medium and did not depend on the external concentration of renin. 2. Although the renin granules were osmotically and mechanically fragile, they were quite stable at 0 degrees C in isotonic medium. 3. The bulk of renin activity appeared in the supernatant when the granules were ruptured by osmotic lysis. About 8% of the total renin still remained in the membrane fraction of the granules after treatment by freezing and thawing. 4. Therefore stored renin in the granules can be described as comprising three components: a readily released soluble form; a soluble but hard-to-release form; a membrane-bound form.
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PMID:Renin release from renin granules in the dog. 66 62

The mechanism and structural basis of the inhibition of renin release by angiotensin II (AII) were studied in rat kidney slices. Renin release was inhibited by AII and the (2-8), (3-8), (4-8), and (5-8) peptides of AII (5 X 10(-5) M). These constituent peptides of AII which share a common carboxyl terminus inhibited renin release with a sharp decrease in potency when the amino-terminal amino acid was removed. Saralasin attenuated the inhibition of renin release induced by equimolar concentrations of AII. Dose-response curves for AII and the (2-8) peptide [angiotensin III (AIII)] indicate that AII is a more potent inhibitor of renin release than is AIII. Depletion of renal norepinephrine by reserpine (10 mg/kg, i.p.) or pretreatment of slices with papaverine (1 X 10(-4) M) did not block the action of AII. The data give evidence for a direct action of AII on the juxtaglomerular cells independent of an interaction with either the sympathetic nervous system or the arteriolar baroreceptor and suggest that the intrarenal receptors that mediate AII-induced inhibition of renin release differ from AII receptors in the adrenal cortex.
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PMID:Inhibition of renin release from rat kidney slices by the angiotensins. 67 19


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