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

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

Homogenates of rabbit renal cortex contained a water-soluble material with striking activity on smooth muscle derived from the rabbit aorta, rat stomach, and guinea pig ileum--but not rat colon or chick rectum. Evidence derived from the spectrum of its pharmacologic activity, the influence of specific competitive antagonists on the smooth muscle responses to the factor, the influence of proteolytic enzymes and its elution position during molecular sieve filtration on Sephadex G-10 made it unlikely that the factor was a prostaglandin, renin, angiotensin, a catecholamine, serotonin, bradykinin, a nucleotide, a small organic product of local metabolism, or a small ion. The agent was not found in extracts of renal medulla, spleen, myocardium, or lung. The smooth muscle response to the factor was blocked by phenoxybenzamine. The renal cortical factor in subthreshold concentration also potentiated responses of the rabbit aorta to angiotensin and norepinephrine. The factor's intrinsic activity and ability to potentiate the smooth muscle actions of endogenous vasoconstrictors make it a candidate as a mediator of smooth muscle responses in a number of states.
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PMID:A smooth muscle active factor isolated from renal cortex of the rabbit. 1 8

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.
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PMID:Effects of calcium on renin and aldosterone in the rat. 1 57

Studies were performed to evaluate the effects of the chronic administration of furosemide on hydrogen and electrolyte excretion in dogs on a normal electrolyte diet and in the absence of electrolyte or volume depletion. Control daily excretion in five dogs averaged 64 meq for Na, 51 meq for K, 66 meq for Cl, and 17 meq for net H. Furosemide, 40 mg, in the drinking water 3 times daily was given for 4 days. On day 1 Na excretion averaged 128 meq, but thereafter was not significantly different from control levels. Over 4 days cumulative net H excretion increased 63.6 meq and plasma HCO3 rose 6.6 meq/liter. The same dogs were restudied by the same protocol except that, to obviate electrolyte depletion, NaCl and KCl were administered daily in quantities sufficient to replace urinary losses. All dogs remained in positive Na, K, and Cl balance. Body weight, hematocrit, plasma albumin, creatinine, and plasma renin activity were unchanged, indicating the absence of electrolyte or volume depletion. Nonetheless, cumulative net H excretion increased 61.2 meq and plasma HCO3 increased 4.3 meq/liter. Two adrenalectomized dogs receiving steroid replacement showed similar changes in net H excretion and plasma HCO3. These experiments suggest that chronic furosemide administration may enhance H excretion and generate alkalosis even in the absence of volume or electrolyte depletion and without increased aldosterone secretion.
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PMID:Effect of chronic furosemide administration on hydrogen and sodium excretion in the dog. 1 99

The beta1- and beta2-components in antidiuresis and sodium retention induced by beta-adrenergic agonists were analysed in ethanol-anesthetized, water-diuretic rats. Intravenous infusions of isoprenaline, salbutamol and carbuterol did not affect insulin clearance but increased plasma renin concentration to the same same extent. Propranolol completely blocked the decreases in urine volume (V) and urinary sodium excretion (UNaV) induced by isoprenaline; practolol (beta1-blocker) inhibited only the decrease in UNaV and butaxamine (beta2-blocker) inhibited only the decrease in V. The ratios of doses of beta-agonists which decreased UNaV and by 50% (ED50 UNaV decrease/ED50 V decrease) were 0.34, 0.68, 1.56 and 2.36 for isoprenaline, tretoquinol, salbutamol and carbuterol, respectively. This increasing order of the ratios coincided with the order reported for the preponderance of the beta2- over beta1-component of these agonists. These results indicate that the decrease in UNaV induced by beta-agonists is related to beta1 stimulation, while the decrease in V is related to beta2 stimulation.
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PMID:Antidiuresis induced by beta1- and beta2-adrenergic agonists in ethanol-anesthetized rats. 2 97

The effect of bilateral renal denervation on water intake and urine volume during specific thirst challenges was studied in rats. Renal denervation attenuated significantly the drinking response elicited by the administration of 30% polyethylene glycol (PG, extracellular challenge) but had no effect on the drinking response after an intracellular challenge (2.5 M NaCl) or after a 24-h water deprivation period. Furthermore, during a PG challenge total water intake was the same in two groups of rats, one with denervated kidneys and the other with beta-adrenergic neural activity in efferent renal nerves eliminated by blocking agents. Urine volumes were not affected by PG administration or water deprivation in denervated rats but were increased significantly after administration of 2.5 M NaCl. These results indicate that renal nerves play an important role in the physiological processes controlling extracellular thirst, and suggest that this role may be related to the neural control of release of renin.
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PMID:The role of renal nerves in the response to dipsogenic stimuli in the rat. 3 May 24

The fact that drinking in response to some hypovolemic stimuli was attenuated by nephrectomy but not by ureteric ligation led to the suggestion that the renal renin-angiotensin system may play a role in hypovolemic thirst. The isolation of a thirst factor from the kidney and the demonstration that this substance was renin supported the hypothesis. Subsequently, it was shown that the effects of renin on drinking were mediated through angiotensin II, which proved to be a potent dipsogenic substance when administered systemically or injected directly into the brain. Recently, it has been shown that angiotensin II, infused intravenously or through the carotid artery at rates that produce increases in plasma angiotensin II levels similar to those that occur in mild sodium depletion, causes the water-replete animal to drink. This discovery establishes that angiotensin is a physiological stimulus to drinking but it leaves open the question of the extent of the involvement of renal renin in normal thirst. Other unsolved problems are the role of cerebral isorenin in angiotensin thirst and its relationship with renal renin, and in view of its stimulating action on sodium intake when infused into the brain, whether angiotensin plays a significant role in sodium appetite.
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PMID:Angiotensin, thirst, and sodium appetite: retrospect and prospect. 3 Jun 50

To evaluate the contribution of chloride to acute renin inhibition by sodium chloride, plasma renin activity (PRA) was measured before and after peripheral venous infusion of NaCl, NaHCO3, NaBr, NaNO3, lysine monohydrochloride, or lysine glutamate in NaCl-deprived rats. In contrast to controls and animals infused with other sodium salts, PRA decreased (P less than 0.01) after infusion with NaCl [from 28.3 +/- 2.8 to 13.3 +/- 1.8 ng/ml per h (SE)] and NaBr (from 40.6 +/- 6.2 to 21.8 +/- 3.9 ng/ml per h), and renal tubular halide reabsorption increased (P less than 0.05). Arterial pressure, plasma volume, inulin clearance, net sodium balance, serum Na+ and K+, and pH were not different among sodium-loaded groups. PRA was also suppressed (P less than 0.01) by infusion with lysine monohydrochloride (from 51.6 +/- 5.4 to 32.4 +/- 5.1 ng/ml per h) but not with lysine glutamate. These results suggest that inhibition of renin by sodium is dependent on an intrarenal effect of chloride. During infusion with sodium salts which suppressed renin, negative free water clearance (TcH2O) increased, whereas infusion with sodium salts that did not inhibit renin resulted in either no change or decreased TcH2O. The association of renin inhibition and increased TcH2O indirectly supports the hypothesis that renin suppression by chloride is related to the magnitude of absorptive chloride transport in the thick ascending limb of the loop of Henle.
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PMID:Importance of chloride for acute inhibition of renin by sodium chloride. 3 96

Angiotensin circulates in the blood as a hormone. Its main target organs are vascular smooth muscle, adrenal gland and the kidney. Hormonal angiotensin increases blood pressure by its vasoconstrictor action, by stimulation of aldosterone secretion and subsequent sodium and water retention, and by the stimulation of catecholamine release. Circulating plasma angiotensin also effects brain mechanisms of blood pressure regulation. In addition to this hormonal function, angiotensin is present in the brain as part of an endogenous brain renin-angiotensin system. Brain angiotensin is not secreted into the blood and can be considered a neurohormone with local function. A role of brain angiotensin in the maintenance of high blood pressure of spontaneously hypertensive rats has been demonstrated. Circulating plasma angiotensin appears to influence brain renin levels and vice versa. Stimulation of specific areas in the brain known to be involved in the regulation of the cardiovascular system, stimulate renin secretion from the kidney. The renin-angiotensin system can therefore serve as an example for the intimate interrelationship between humoral and neurohumoral mechanisms of blood pressure regulation.
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PMID:Humoral and neurohormonal aspects of blood pressure regulation: focus on angiotensin. 3 33


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