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)

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

Tubuloglomerular feedback has been defined as a mechanism in which changes in distal tubular sodium chloride delivery induce changes in glomerular arteriolar resistance. Experiments were performed in rats to test the hypothesis that the alterations in vasomotor activity are controlled by local hormonal mechanisms. Early proximal flow rate (EPFR), used as an index of filtration rate, was assessed at loop perfusion rates of 10 and 40 nl/min and during zero loop flow before and during intravenous administration of agents which interfere with the reninangiotensin or adrenergic systems. During infusion of the angiotensin (A) antagonists [Sar1,Ile8-]-AII or [Me2,Gly1,Ile8]-AII at doses ranging from 4.8 to 30.6 micrograms/kg . min, feedback response, expressed as percent change of EPFR during loop flow elevation from 3 to 40 nl/min, fell from a mean of 47.6 +/- 3.3% to 33.2 +/- 2.9% (P less than 0.05). Likewise, after administration of the converting enzyme inhibitor SQ 20881 in a dose ranging between 5.5 and 34.0 mg/kg, feedback response decreased from 48.5 +/- 2.1% to 25.9 +/- 1.9% (P less than 0.001) and returned to 43.1 +/- 5.1% after the inhibitory effect of SQ 20881 on the pressure response to angiotensin I had disappeared. Luminal application of [Sar1,Thr2]-AII (5mM) or of SQ 20881 (5 or 10 mM) had no effect on the feedback response. A significant reduction in the feedback response was noted also during intravenous infusion of propranolol (46.4 +/- 3.2% vs. 29.0 +/- 2.8%, P less than 0.001), whereas 6-OH-dopamine, reserpine, or phenoxybenzamine had no detectable effect. Our results are in agreement with the concept that the renin-angiotensin system may mediate feedback-induced resistance changes. In addition, circulating catecholamines may, in some unknown manner, act as modulators of the feedback response.
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PMID:Feedback regulation of nephron filtration rate during pharmacologic interference with the renin-angiotensin and adrenergic systems in rats. 3 87

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

Conscious Merino ewes were given an intravenous hypertonic sodium chloride load of 4 mmol.min-1 for 100 min. This resulted in increases in urine flow, sodium and potassium excretion and plasma sodium concentration and osmolality. Urinary vasopressin output and solute-free water reabsorption increased and plasma renin activity declined. Renal plasma flow and glomerular filtration rate (GFR) rose, as did the solute clearance. The change in urinary osmolality was related to the initial urine osmolality such that when the initial urine osmolality was high the urine became more dilute, and vice versa. Tubular sodium reabsorption increased but the fractional reabsorption rate fell. It is suggested that the increase in GFR was at least partly due to the increase in AVP and that the electrolyte loss can be accounted for by the increase in GFR without necessarily involving AVP or other hormonal effects at the tubular level.
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PMID:The effect of intravenous hypertonic saline infusion on renal function and vasopressin excretion in sheep. 25 75

It has been shown that the severity of experimentally induced acute renal failure (ARF) is inversely related to dietary sodium chloride intake, and the effects have been attributed to the concurrent changes in renal renin. In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. In two nephrotoxic models (mercuric chloride, uranyl nitrate), giving previously sodium-deprived rats 1% sodium chloride to drink for 48 hours prior to ARF induction greatly attenuated the severity without any reduction in their high renal renin. Conversely, giving previously sodium-loaded rats tap water to drink for 4 to 5 days prior to AFR induction greatly enhanced the severity without any increase in their subnormal renal renin. Therefore, the changes in severity of ARF resulting from changes in dietary sodium are not mediated by changes in renal renin. Significant inverse correlations were found between mean peak BUN values during the follow-up period (5 to 7 days) and the 24-hour urinary sodium excretions prior to ARF induction in both models, suggesting that sodium intake and/or excretion at the time of induction is a good predictor of the severity. The effects of sodium chloride in both models were predominantly expressed during the maintenance phase, and consisted of attenuation of the severity (both models) and hastening of the recovery (mercuric chloride model). Possible mechanisms by which dietary sodium produced its effects, independently of its effects on the renin-angiotensin system, are discussed.
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PMID:Sodium-chloride-induced protection in nephrotoxic acute renal failure: independence from renin. 39 16

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

1. Angiotensin II (ANG II) was measured in acid-ethanol homogenates of rapidly frozen rat kidneys by a method involving ion-exchange and immunoadsorbent purification of peptides before radioimmunoassay. 2. Concentrations of ANG II found in kidney were 10--20 times that in plasma. 3. Perfusion of the kidneys via the renal artery with isotonic sodium chloride solution or with disodium EDTA solution did not alter the concentrations of intrarenal ANG II. 4. Animals fed on a sodium-deficient diet for 8 days had markedly higher concentrations of intrarenal ANG II, plasma renin activity and kidney renin concentration than sodium-replete animals. 5. After oral sodium loading for 3 weeks, rats had suppressed plasma renin activity and kidney renin concentration but unchanged intrarenal ANG II when compared with animals on a normal sodium intake. 6. One hour after the administration of a converting enzyme inhibitor (SQ 20881) plasma renin activity was elevated, kidney renin concentration unchanged and intrarenal ANG II was depressed. 7. These results demonstrate the presence of ANG II in the extravascular compartment of the kidney. They further suggest that its quantity is influenced by sodium intake and that angiotensin I converting enzyme is essential for its formation.
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PMID:Evidence for the local occurrence of angiotensin II in rat kidney and its modulation by dietary sodium intake and converting enzyme blockade. 47 54

After an ischaemia lasting 1 hour as well as after an extreme hypertension lasting 210 minutes in the kidney of a rat a significant increase of the renin activity in the juxtaglomerular apparatus was found. By chronic load with sodium chloride was tried to produce a decrease of renin. In contrast to an ischaemic lesion the kidneys of the animals loaded with salt revealed a better ischaemia tolerance than those of the unloaded animals. This is expressed by a significantly increased total blood supply and cortical blood supply. On the two experimental conditions a change of the distribution of the blood supply in favour of the inner compartments of the kidneys may be observed. In the oxygen histogram of the surface of the kidney the salt-loaded kidneys reveal a better oxygenation before and after the ischaemic lesion. The kidneys loaded before show an essentially more insignificant decrease of the urine excretion than the unloaded ones.
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PMID:[Chronic sodium chloride load--a possibility for the increase of tolerance for ischemia in the kidney]. 48 65

Biochemical investigations in a boy with a salt losing syndrome revealed a very low secretion of aldosterone which did not rise during salt deprivation, in spite of a normal rise in plasma renin activity. Cortisol secretion was normal - but subsequently decreased, while the corticosterone secretion was high. The patient was studied at the age of 5 weeks, 3 months and also at the age of 8 months. He survived until the age of 18 months on treatment with sodium chloride and DOCA, but did not receive glucocorticoids. At autopsy the adrenal glands were absent, but in fat tissue from the upper renal poles foetal adrenal cortex tissue was found. The histological picture agrees well with other cases which could be designated as "foetal-cortex-only" adrenal hypoplasia. The same histological changes were demonstrated in the boy's brother who died suddenly at the age of 6 weeks. The boy's testes were advanced in maturation to a stage of about ten years: spermatocytes and Leydig cells were present.
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PMID:Familial adrenocortical hypoplasia with early clinical and biochemical signs of mineralocorticoid deficiency (hypoaldosteronism). 57 34

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.
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PMID:Decreased plasma renin activity and renin release in rats with phaeochromocytoma. 58 29


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