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)

In healthy male subjects aldosterone excretion and plasma renin activity were reduced by a 4-6 hr head-out immersion in thermoindifferent water baths (35.5 +/- 0.1 degrees C). The red cell 2,3-diphosphoglycerate (DPG) concentration before and throughout immersion period was positively correlated both with aldosterone excretion in 2 hr pooled urine (r = +0.69; 2 p less than 0.001) and with renin activity (r = + 0.54; 2p less than 0.001) despite a concomitant increase of cubital venous pH and inorganic phosphate concentration. These findings furnish evidence for a regulatory role of aldosterone in DPG metabolism, possibily by a direct influence on red cell glycolysis.
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PMID:Some evidence for aldosterone action on 2,3-diphosphoglycerate level in human red cells. 0 30

The effect of 24 h of unilateral ureteral obstruction on HCO3 reabsroption and urinary acidification was studied in dogs. The postobstructed kidney (EK) had a significantly lower glomerular filtration rate and renal plasma flow than the contralateral kidney (CK). Urinary pH prior to HCO3 loading was significantly higher in the EK as was maximal HCO3 reabsorption. Saline loading depressed HCO3 reabsorption to the same degree in both kidneys. Urinary PCO2, during HCO3 loading, and during phosphate infusion, was significantly lower in the EK than the CK. Fractional Na excretion was significantly higher in the EK than the CK after deoxycorticosterone acetate administration. Na2SO4 administration enhanced acid excretion only in the CK. K excretion was significantly lower in the EK than the CK both during HCO3 loading and Na2SO4 administration. There was redistribution of cortical blood flow from the outer cortex toward the inner cortex in the EK as compared to the CK. There was no difference in plasma renin activity from both renal veins. These data demonstrate enhanced proximal H+ secretion (which is abolished by volume expansion) and impaired distal H+ secretion by the postobstructed kidney. The distal defect is likely an effect of a generalized disorder of distal transport in that both K secretion and steroid-responsive Na reabsorption were impaired in the postobstructed kidney.
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PMID:Renal hydrogen ion secretion after release of unilateral ureteral obstruction. 1 Jul 40

The interaction between parathyroid hormone (PTH) and the renin-angiotensin system was evaluated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH (1-34) for 1 h was accompanied by a 57% increase (13.7-21.6 ng/ml per h) in plasma renin activity (PRA) which returned toward control levels during the recovery period. Sodium and phosphate excretion also increased. Second the endogenous secretion of PTH was stimulated by infusion of citrate into the blood supply of the thyroparathyroid glands to determine if the stimulatory effect on renin occurred with endogenous secretion of PTH. Phosphate excretion increased, which confirmed PTH secretion. There was a significant rise (57%) in both PRA (6.1-9.8 ng/ml per h) and sodium excretion, the magnitude of the sodium response modulating the increase in PRA. Blood pressure remained constant. In a third set of experiments, thyrocalcitonin was infused intravenously and had no effect on PRA. These data indicate that both exogenous and endogenous PTH can elevate PRA and increase sodium excretion. The sodium effect is probably the result of inhibition of proximal sodium reabsorption by PTH. The mechanism by which PTH elevates PRA is not known.
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PMID:Effect of parathyroid hormone on plasma renin activity and sodium excretion. 42 73

The effect of thyroid hormone on renin productiona and release by rat kidney slices was studied. Rat kidney slices were incubated in Warburg flasks containing Krebs-Ringer-Phosphate- Glucose- Dextran solution at 37 C for 5 hours. Renin content, renin released into the incubation media and oxygen consumption were measured. Kidney slices actively secreted renin. Kidney slices of hyperthyroid rats released more renin, and kidney slices of hypothyroid rats released less renin than normal kidneys (p less than 0.001). The addition of 1-thyroxine to the incubation medium increased significantly (p less than 0.001) renin release by kidney slices from normal and hypothyroid rats. Thyroid hormone affects renin release through a mechanism independent of the ouabain-sensitive sodium pump and protein synthesis, since ouabain and cycloheximide did not modify renin release or production. The results of this study suggest that thyroid hormone plays a role in renin release from the juxtaglomerular cells.
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PMID:The effect of thyroid hormone on renin production and release by rat kidney slices. 61 72

Studies were carried out in anesthetized dogs to characterize the increase in cation excretion which occurs after acute unilateral nephrectomy (AUN). 60 min after AUN, cation excretion had increased from 31.5+/-2.7 to 66.3+/-12.0 mueq/min (P < 0.005) and fractional cation excretion had increased from 0.56+/-0.05 to 1.03+/-0.14% (P < 0.005), as the glomerular filtration rate was unchanged and renal blood flow fell. The increased cation excretion was accompanied by an increase in fractional phosphate excretion, no change in chloride excretion, and a fall in renin secretion. These alterations in renal function were associated with marked changes in systemic hemodynamics: cardiac output fell from 2.52+/-0.24 to 1.85+/-0.16 liters/min (P < 0.001), as diastolic pressure rose without an overall increase in mean arterial pressure, and heart rate fell. To assess the importance of these hemodynamic changes in the renal response, AUN in a separate group of dogs was accompanied by the simultaneous opening of a surgically created femoral artery-to-vein fistula at flow matching the blood flow to the removed kidney. When this was done, no alterations in systemic or renal hemodynamics were observed, and cation excretion did not differ from control. Subsequent closure of the fistula then caused a fall in cardiac output from 2.15+/-0.25 to 1.77+/-0.20 liters/min (P < 0.05), and an increase in cation excretion from 34.6+/-9.5 to 52.3+/-13.7 mueq/min (P < 0.01), thus mimicking the findings with AUN alone.These results demonstrate that AUN causes hemodynamic changes resembling those seen on closure of a chronic arteriovenous fistula. Prevention of these hemodynamic changes after AUN also prevents the functional adjustment of the remaining kidney, suggesting that they may be important in initiating the renal response. The increased electrolyte excretion after AUN may occur through mechanisms similar to that seen on closure of an arteriovenous fistula.
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PMID:Role of hemodynamic changes in the increased cation excretion after acute unilateral nephrectomy in the anesthetized dog. 64 Nov 40

The denervation diuresis and natri uresiswere manifest in anesthetized dog and rats after acute or chronic renal sympathectomy with no changes in RBF, GFR or in their intrarenal distribution. Micropuncture showed the principal site of action of renal denervation on to be within the proximal tubule. The unchanged relationship between reabsorbed sodium and consumed oxygen suggested that active transport of Na decreased on denervation. No causal relationship between denervation natri uresis and decreased release of renin was revealed. As tubular transport of d-glucose, inorganic phosphate, para--aminohippurate and of uric acid was suppressed by the sympathectomy, the renal sympathetic activity seem to be able to regulate the proximal tubular transport functions.
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PMID:[Neural regulation of substance transport in the kidney]. 64 63

Renin substrate was initially extracted from human plasma by (NH4)2SO4 followed by chromatography on Sephadex G-150, DEAE cellulose, calcium phosphate gel, isoelectric focusing and preparative polyacrylamide gel electrophoresis. On the basis of one mol of angiotensin per mol of substrate, the purity of the preparation is in excess of 95%. On analytical polyacrylamide gel electrophoresis in the presence of 1% sodium dodecyl sulfate or 8 M urea, the protein appears homogenous. In addition, the purified protein shows only one preciptin line against anti-normal human serum on either Ouchterlony immunodiffision or immunoelectrophoresis. The biological activity appears similar to "native" renin substrate since the Km is the same as that reported for the renin reaction in whole plasma. The molecular weight was determined as 110 000 by gel filtration and polyacrylamide gel electrophoresis; amino acid analysis of the human substrate differs from that reported for hog, especially in the Asp, Glu and Gly composition.
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PMID:Purification and partial characterization of human angiotensinogen. 81 79

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

In three patients with Bartter's syndrome, indomethacin administration resulted in the disappearance of the hypokalemic alkalosis and in a normalization of the elevated plasma renin activity. Changes in calcium and phosphate metabolism during indomethacin medication seemed to indicate an increase in reabsorption activity of the renal proximal tubulus. A kidney biopsy performed in one of the patients showed, besides hyperplasia of juxtaglomerular cells, hyperplasia of interstitial medullary cells which are presumed to produce prostaglandins. As indomethacin is a well-known inhibitor of prostaglandin synthesis, the observations suggest that an overproduction of renal prostaglandins could well be of pathogenetic significance in Bartter's syndrome.
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PMID:Indomethacin in Bartter's syndrome: does the syndrome represent a state of hyperprostaglandinism? 91 67

1. The effects of different energy substrates, of low temperature, of urea, and of ouabain and ethacrynic acid were studied on the rate of renin release from viable juxtaglomerular cells during superfusion of isolated rat glomeruli. 2. Neither lactate nor glutamate altered renin release rate from that observed using glucose as the sole energy substrate. Succinate 10 mM elevated release transiently but did not influence the release caused by reductions in osmolality through lowering sucrose concentration. 3. Peak renin release was more prolonged and returned more slowly to control following reductions in osmolality in phosphate-Ringer than in bicarbonate-Ringer. 4. At 37 degrees C, the peak of renin released induced by hypo-osmolality was smaller and delayed, and returned earlier to control than at 30 degrees C. Reduction in temperature from 30 to 4 degrees C resulted in a 32-fold increase in basal release rate. At 4 degrees C a 20 m-osmole/kg reduction in tonicity caused an additional 2-5-fold increase in release rate. 6. Increasing superfusate osmolality with urea did not affect basal renin release but 100 mM urea suppressed the releasing effect of a 15 mM reduction in NaCl concentration. 7. Ouabain (10(-4) M) caused a small (33 +/- 9%, P less than 0-025) transient increase in renin release. Ethacrynic acid (10(-3) M) provoked a progressive increase in release reaching 100 +/- 15% above control within 50 min. In the presence of both inhibitors the release provoked by hyposmolality was prolonged. 8. It is concluded that renin release in vitro is a function of actively regulated cell volume and it is proposed that a similar mechanism could underline both barorecptor and macula densa controls of renin secretion in vivo.
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PMID:Studies on renin release from isolated superfused glomeruli: effects of temperature, urea, ouabain and ethacrynic acid. 94 62


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