Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of the effect of somatostatin (growth-hormone release-inhibiting hormone) on plasma-renin in healthy volunteers, plasma-renin activity was measured by radioimmunoassay after the intravenous administration of somatostatin and also during frusemide-induced hyperreninaemia. While somatostatin was being given, basal values of renin were unchanged. Injection of frusemide alone produced hyperreninaemia; but, under somatostatin, renin release was inhibited by 45%. The results indicate that somatostatin is a potent inhibitor of renin and exerts its effect independent of sodium excretion, which was unchanged under somatostatin. Conceivably, somatostatin plays an important role in the regulation of endogenous renin release.
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PMID:Inhibition of frusemide-induced hyperreninaemia by growth-hormone release-inhibiting hormone in man. 5 89

Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. In pharmacological dosage, gastric acid output, splanchnic blood flow and plasma renin levels, are influenced. A possible therapeutic effect on increased growth hormone secretion, disturbances of carbohydrate metabolism, gastroenteropathies and renal hypertension, is discussed. The clinical application is limited by the short biological half-life of the substance and the unspecific action on several organs.
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PMID:[Somatostatin]. 37 88

Intravenous infusion of somatostatin in mongrel dogs caused a significant decrease in the peripheral plasma renin activity (PRA) enhanced by pentobarbital sodium anesthesia or furosemide treatment. However, the inhibitory activity vanished within 10 min after termination of somatostatin infusion. Intrarenal arterial infusion of somatostatin decreased furosemide-enhanced PRA in renal vein by 24.0%, 16.6% and 8.6% in dose of 0.1, 0.5 and 1.0 microgram, respectively. On the other hand, high doses of the peptide (50-200 microgram) failed to decrease. The changes in PRA occurred in the absence of any alteration in blood pressure during the intravenous infusion under furosemide treatment. In an in vitro study, the addition of somatostatin in doses of 0.01 and 0.05 microgram suppressed the renin release in dog renal cortical cell suspension by 74.3% and 53.6%, respectively. Therefore, in both intrarenal arterial infusion and the cell suspension system, somatostatin was increasingly effective in decreasing renin release towards the lower end of the dose range tested. These results suggest that the effect of somatostatin on hyperreninemia may involve an inhibition of renin release at the cell level in the kidney.
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PMID:Effect of somatostatin on plasma renin activity. 47 26

In the anaesthetized rat synthetic somatostatin can interfere with the renin-angiotensin system by increasing plasma renin activity and decreasing normal blood pressure or counteracting several types of experimental hypertension.
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PMID:Influence of somatostatin on blood pressure and plasma renin activity in the rat. 58 59

The interrelationships of increased plasma renin and elevated blood pressure following acute beta-stimulation by orcipernaline and its prevention by somatostatin was studied in normal man. During somatostatin infusion basal values of renin and blood pressure were unchanged. Following orciprenaline both variables increased significantly. Combination of somatostatin and orciprenaline reduced the rise in plasma renin activity by 49%, mean arterial blood pressure by 21% and heart rate by 19%, compared with beta-stimulation alone. The results indicate that the inhibitory action of somatostatin on plasma renin activity may be mediated via beta-receptors. The lesser increase of blood pressure under somatostatin plus orciprenaline also indicates a possible inhibitory effect of somatostatin on beta-adrenergic receptors.
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PMID:Prevention by somatostatin of rise in blood pressure and plasma renin mediated by beta-receptor stimulation. 88 78

The effects of tetradecapeptide somatostatin on renin secretion has been studied in the isolated perfused kidney of the rat. The stimulation mediated by isoproterenol (7 X 10(-9) M), theophylline (10(-4) M) and PGE2 (10 ng/ml) was not inhibited by somatostatin (75 ng/ml).
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PMID:[Effect of somatostatin on renin secretion in the isolated perfused rat kidney (author's transl)]. 93 18

Administration of growth hormone-release inhibiting hormone (GH-RIH, somatostatin), as a 90 minute infusion (10 mug/min), to 3 healthy young men under conditons of active renin secretion acheived by pretreatment with furosemide (80 mg daily for 5 days), caused a mean 30% fall in plasma renin activity, which returned to basal levels immediately after stopping the GH-RIH infusion. Plasma aldosterone levels were not affected during the course of this experiment.
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PMID:Actions of growth hormone-release inhibiting hormone (somatostatin) on the renin aldosterone system. 94 43

To investigate the renal effects of somatostatin in cirrhosis, renal function and plasma and urinary levels of endogenous neurohumoral vasoactive substances were measured in conditions of intravenous water overload (20 mL/kg body wt with 5% glucose) before and during the intravenous infusion of somatostatin (250-500 micrograms/h) in 6 cirrhotic patients without ascites and 17 nonazotemic cirrhotic patients with ascites. Somatostatin induced a significant reduction of renal plasma flow, glomerular filtration rate, and free water clearance in both groups of patients. In patients with ascites, somatostatin also reduced urinary sodium excretion. Changes in renal function were significantly more marked in patients with ascites than in those without ascites and occurred in the absence of changes in mean arterial pressure and plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide. Somatostatin induced a significant reduction in the plasma concentration of glucagon and urinary excretion of prostaglandin E2 that was not related to changes in renal function. These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems.
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PMID:Effects of somatostatin on renal function in cirrhosis. 809 52

Increasing evidence indicates that angiotensin II can be formed by juxtaglomerular cells (JGC) and cosecreted with renin. We investigated the existence of this local renin-angiotensin system in a human JGC tumor, using an in vitro superfusion. The JGC tumor was found concomitantly to release renin and angiotensin I and II. Sequential addition of atrial natriuretic peptide, dopamine, and a somatostatin analog in the superfusion did not affect renin or angiotensin I and II release. The data provide evidence that the human JGC tumor in vitro generates angiotensin II, and supports its possible role as a local in vivo regulator of kidney function.
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PMID:Concomitant release of renin, angiotensin I, and angiotensin II during superfusion of human juxtaglomerular cell tumor. 138 67

The acute effects of i.v. somatostatin (250 mcg bolus followed by 250 mcg/h continuous infusion for two hours) on renal hemodynamics, renal electrolyte and water handling, and urinary excretion of catecholamines and prostaglandins, as well as on plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, dopamine, glucagon, and plasma renin activity were studied in seven normal subjects. Somatostatin decreased effective renal plasma flow and glomerular filtration rate, osmotic and free water clearances, urine volume, and sodium and potassium excretion, while urinary osmolality, fractional excretion of sodium, and phosphate excretion increased significantly. Plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, and dopamine remained unchanged, while plasma renin activity (3.0 +/- 0.25 vs 2.4 +/- 0.2 ng AngI/ml/h; p less than 0.01) and glucagon levels (40 +/- 11 vs 20 +/- 16 pg/ml; p less than 0.01) decreased. Urinary excretion of norepinephrine, epinephrine, dopamine, PGE2, and PGF2 alpha was suppressed under somatostatin. A significant positive correlation was found between urinary dopamine and sodium excretion (r = 0.7; p less than 0.001) and urinary prostaglandin E2 and glomerular filtration (r = 0.52; p less than 0.01). Without accompanying changes in plasma osmolality and vasopressin concentration significant antidiuresis occurred, suggesting a direct tubular effect of somatostatin. However, the hormone-induced changes are due mainly to the decrease in renal plasma flow. The results demonstrate that somatostatin at supraphysiological doses exerts significant effects on the kidney.
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PMID:Effect of somatostatin on kidney function and vasoactive hormone systems in health subjects. 168 Nov 32


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