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)

1. The effect of intravenous loading with 500 ml of sodium chloride solution (50 g/l) on plasma renin concentration, plasma aldosterone concentration, urinary sodium excretion and mean blood pressure was studied in 15 young patients with mild essential hypertension and 10 healthy normotensive control subjects. 2. Plasma renin concentration and plasma aldosterone concentration were suppressed to the same degree during loading in both the hypertensive and normotensive groups. Urinary sodium excretion was significantly higher in the hypertensive patients than in the normotensive subjects. Mean blood pressure increased slightly in both groups. 3. Plasma renin concentration and plasma aldosterone concentration were significantly correlated in both groups before sodium loading. The increase in urinary sodium excretion was significantly correlated to the suppression of plasma aldosterone concentration in the hypertensive, but not in the normotensive, group. No correlation was found between changes in urinary sodium excretion and changes in plasma renin concentration or mean blood pressure. 4. The results indicate that the suppressibility of the renin-aldosterone system by hyperosmotic sodium chloride solution is normal in young patients with mild essential hypertension. It is suggested that the changes in plasma aldosterone concentration induced by sodium loading might be involved in the regulation of exaggerated natriuresis in essential hypertension.
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PMID:The renin-aldosterone system in exaggerated natriuresis of essential hypertension. 58 41

We previously have shown that chronic sodium chloride (NaCl) loading protects against HgCl2-induced acute renal failure (ARF) in dogs. To determine whether NaCl loading protects against an ischemic model of ARF, unilateral oliguric renal failure was produced by the infusion of norepinephrine (NE) into the renal artery of both saline-expanded (SE) and water-drinking (WD) dogs (n = 7). The renal renin content (30 U/g kidney) of SE dogs was suppressed (P less than 0.001) compared to that of WD dogs (132 +/- 18). Forty-eight hours after infusion of NE (1.5 microgram/kg per min X 100 min), inulin clearances from the infused kidney of SE (6 ml/min +/- 2) and WD dogs (7 +/- 2) did not differ; in both groups, respective clearances from the noninfused kidney (43 ml/min +/- 3) and (36 +/- 5) also did not differ from each other. The present fall in renal blood flow to the infused kidney 48 hours after NE in SE (44%) and WD dogs (38%) did not differ. Because of failure to demonstrate protection, a lower dose of NE (0.75 microgram/kg per min X 40 min) was infused into SE and WD animals (n = 6). Forty-eight hours after low dose NE, inulin clearances of the infused kidney of SE (17 ml/min +/- 5) and WD dogs (17 +/- 4) did not differ. Respective clearances in the noninfused kidney of SE (46 ml/min +/- 6) and WD dogs (35 +/- 4) did not differ. Therefore, despite suppression of renal renin content, NaCl loading failed to protect against this ischemic model of ARF. In conclusion, unlike HgCl2-induced ARF, it is unlikely that the renin angiotensin system contributes to the pathogenesis of this ischemic model of ARF.
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PMID:Failure of chronic sodium chloride loading to protect against norepinephrine-induced acute renal failure in dogs. 61 99

A boy with pseudohypoaldosteronism was followed from birth to the age of 7 years. Failure to thrive, vomiting, dehydration, hyponatraemia and urinary sodium loss were prominent findings. Urinary excretion of corticosteroid metabolites was normal. Before treatment, excessively high plasma renin concentration was found, associated with a marked activation of aldosterone secretion. A renal biopsy showed pronounced hypertrophy of the juxtaglomerular apparatus. Persisting metabolic acidosis and an insufficient urinary acidifying capacity suggested the presence of distal renal tubular acidosis. Treatment with sodium bicarbonate and sodium chloride from 19 to 31 months of age resulted in normal growth and normal physical and mental development. The plasma electrolytes were normalized but a pronounced activation of the renin-aldosterone system persisted after therapy, and on sodium restriction this system responded with a considerable further activation.
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PMID:Pseudohypoaldosteronism. Clinical, biochemical and morphological studies in a long-term follow-up. 62 83

The renin-angiotensin system, ACTH and hyperkalaemia are known to induce increased plasma levels of aldosterone. In order to assess the relative significance of these mechanisms during surgical stress, aldosterone, cortisol and electrolytes in plasma were measured in 12 otherwise healthy women during and after cholecystectomy. The patients received either isotonic sodium chloride or 5 per cent glucose in water during the experimental period of 22 h. The results showed that the pronounced increase of aldosterone and the concomitant decrease of sodium in plasma found in patients given glucose in water could almost be inhibited by the administration of saline. Cortisol and potassium concentrations were identical in the two groups of subjects. It is concluded that the aldosterone response to surgery is mainly mediated via the renin-angiotensin system. This response is probably due to a reduced sodium content or volume of extracellular fluid, since it could almost be inhibited by administration of sodium chloride. The rationale of saline restriction during and after surgery is questioned.
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PMID:Inhibition of aldosterone response to surgery by saline administration. 63 42

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

A newborn boy (birth weight 2550 g) presented from the first days of life with poor drinking, moderate vomiting and persistent weight loss. On hospital admission at age 4 weeks, there were severe dehydration, dystrophy and electrolyte disturbances (Na 107, Cl 80, K 5,4 mval/l). The usual causes of salt wasting were excluded, but plasma renin activity, plasma aldosterone and urinary aldosterone-18-glucuronide were markedly increased. DOCA had no salt-retaining effect, but a sodium chloride supplement of 3 g per day improved the clinical condition dramatically and normalized the electrolyte values. With this treatment, plasma renin activity and aldosterone were normal or almost normal beyond the age of 6.5 months, but urinary aldosterone-18-glucuronide remained slightly increased. Considerable augmentation of the plasma renin activity and of urinary aldosterone-18-glucuronide, but no clear salt loss were induced by spironolactone. With salt restriction, there was evidence for marked salt loss. Its progress could be inhibited by administration of indomethacin. Since indomethacin inhibits the synthesis of prostaglandins with saluretic activity, it is probable that the prostaglandins participate in the pathogenesis of the salt wasting in pseudohypoaldosteronism.
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PMID:Congenital pseudohypoaldosteronism: case report and review. Effect of indomethacin during sodium chloride depletion. 65 59

1. When marsupial brush-tailed possums were maintained on a normal fruit and vegetable diet with access to water ad libitum, I.V. infusion of synthetic angiotensin II at rates of 0.035-3.5 mug/kg. min caused short-latency drinking in up to seven of eleven animals tested. These rates also had significant pressor effects.2. There was a positive correlation between the rate of angiotensin infusion and the percentage of tested animals which responded by drinking, as well as the amount of water drunk by such animals. The amount drunk during a second infusion 1 hr later was reduced. There was a negative correlation between the rate of infusion and the latency to drinking.3. Of six animals given access to both water and 1.8% sodium chloride solutions, five drank some saline during maintenance and control periods and all responded with short-latency drinking of water to infusion of angiotensin II at 0.35 mug/kg. min.4. Withdrawal of 10% of blood volume, known to stimulate renin production in the possum, caused an increase in water intake in only one of six possums.5. Infusion of isoprenaline I.V. at 20 mug/kg. min, which caused a profound fall in B.P., had no effect on drinking by all six possums.6. It is concluded that these marsupials share with eutherian mammals responsiveness to a dipsogenic action of angiotensin II, which appears to be inhibited by preceding ingestion of water and potentiated by preceding ingestion of hypertonic saline. The physiological significance of this effect is uncertain.
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PMID:The effect of intravenous infusion of angiotensin II on drinking in the Australian marsupial Trichosurus vulpecula. 69 Sep 40

The interrelationships of renal cortical renin content RCRC, sodium chloride excreting and the severity of renal failure were studied in the glycerol-induced acute myohemoglobinuric renal failure model in the rat. Protocols were designed to increase sodium chloride excretion without necessarily resulting in RCRC depletion. Our data fail to demonstrate a relationship between RCRC and severity of renal failure, but they demonstrate an excellent inverse correlation between the sodium chloride excretion of the animals in the 24 h prior to glycerol administration and the severity of resulitng renal failure. The protection of long-term saline-drinking animals should properly be ascribed to the associated natriuresis which develops much before RCRC depletion during the time course of saline drinking. The exact mechanism by which natriuresis exerts its protective effect needs further elucidation, but our data argue against a major role for RCRC in the pathogenesis of acute experimental renal failure.
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PMID:Natriuresis-induced protection in acute myohemoglobinuric renal failure without renal cortical renin content depletion in the rat. 74 Jan 14

Severe constriction of the suprarenal abdominal aorta of 3-kg rabbits to 3.7+/-0.2 mm2 and maintenance of a daily sodium intake of 10 mE q by infusion of 0.9% sodium chloride resulted in a progressive increase in central ear arterial pressure to 106+/-3 (SEM) mm Hg (control=79+/-1). This was accompanied by a progressive increase in left ventricular end-diastolic pressure to 22+/-2 mm Hg (control=3+/-1), plasma renin activity to 21+/-5 ng of angiotensin/hour per ml (control=5+/-1), plasma aldosterone concentration to 99+/-23 pg/ml (control=14+/-4), and plasma sodium concentration to 142+/-1 mEq/liter (control=136+/-1). Urinary excretion of sodium decreased to 3.9+/-0.7 mEq/day and marked fluid retention occurred. We also found that these changes were accompanied by a decrease in hematocrit to 24+/-2% (control=40+/-1), formation of 36+/-9 ml of fluid in the thoracic cavity, 33+/-9 ml of ascites, pulmonary congestion and edema, hepatic congestion, and enlargement and hypertrophy of both the left and right ventricles. All rabbits died of ventricular failure at a time that was partly related to the degree of aortic constriction and that ranged from 2 to 12 days. The model we have established is chronic, highly reproducible, easy to produce, and inexpensive, and resembles the clinical syndrome of right and left congestive heart failure in man. Furthermore, the studies provide evidence for an important role of the renin-angiotensin-aldosterone system in the fluid retention that leads to pulmonary and systemic venous congestion after suprarenal aortic constriction.
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PMID:The renin-angiotensin-aldosterone system in rabbits with congestive heart failure produced by aortic constriction. 83 74

1. The intrarenal role of angiotensin II in controlling sodium excretion was examined in anaesthetized, dehydrated dogs by infusing the angiotensin II antagonist Sar1-Ile8-angiotensin II directly into the renal artery. Comparisons were made with dehydrated dogs receiving only sodium chloride solution intrarenally. 2. Intrarenal angiotensin II blockade resulted in significant increases in urinary sodium excretion and urine flow rate. 3. The results indicate that during the high-renin state of dehydration endogenous angiotensin II has intrarenal effects which lead to salt and water retention.
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PMID:Intrarenal role of angiotensin II in controlling sodium excretion during dehydration in dogs. 86 48


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