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)

The renal effect of cyclic somatostatin was studied on healthy subjects. The somatostatin was used at therapeutical dose in intravenous infusion. Somatostatin decreases the renal plasma flow, glomerular filtration rate, osmotic and free water clearances, sodium and potassium excretion and the tubular reabsorption of phosphorus while urinary osmolality increases. Under somatostatin infusion the urinary excretion of catecholamines, PGE2, PGF2 alfa and the plasma renin activity and the plasma concentration of glucagon and growth hormone decrease. The antidiuretic activity of somatostatin is due to a) a direct haemodinamic effect, b) an influence on the renal tubular transport as well and also c) because of change the water handling in the collecting ducts.
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PMID:[Effect of somatostatin on kidney function]. 168 89

In the second part of this review concerning adrenocortical growth factors, the following stimulatory agents are included: renin, angiotensin II, atrial natriuretic factor (ANF), prostaglandins--in vivo, fibroblast growth factor (FGF), epidermal growth factor (EGF), adrenal growth factor (AGF) and adrenergic innervation. Furthermore, some growth-inhibiting factors are discussed, as follows: prostaglandins--in vitro, somatostatin, melatonin and N-acetylserotonin.
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PMID:[Factors stimulating and/or inhibiting the growth processes in the adrenal cortex. II. The role of the renin-angiotensin system, tissue growth factors, pineal indole amines and the nervous system]. 168 10

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

A hypotensive effect of an orally-administered cyclopeptide somatostatin analog, MK-678, has been demonstrated in a hypertensive diabetic rat model. Sustained blood pressure reduction failed to occur when the drug was administered to the spontaneously hypertensive rat. The mechanism of hypotension appears independent of effects on a variety of hormones including insulin, glucagon, growth hormone, and components of the renin-angiotensin system including renin activity, plasma angiotensin converting enzyme, and aldosterone.
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PMID:Blood pressure reduction in hypertensive-diabetic rats by the somatostatin analog MK-678. 256 53

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.
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PMID:[Hormonal disorders in borderline arterial hypertension]. 257 58

Hypertension in the obese may be related to hyperinsulinaemia. To investigate this relationship further, we infused somatostatin (250 micrograms/h in 100 ml saline) or saline, single-blind and in a random order, for 10 h in seven obese hyperinsulinaemic hypertensive patients and in seven normo-insulinaemic hypertensive controls. Every 2 h, blood pressure, plasma insulin, glucose, sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were determined. Two hours after the somatostatin infusion was started, mean arterial blood pressure was significantly reduced in the obese hyperinsulinaemic patients (from 128 +/- 11 to 114 +/- 11 mmHg, P less than 0.05) but not in the controls and this reduction persisted throughout the study. The somatostatin infusion reduced plasma insulin and increased plasma glucose similarly in both groups. Plasma sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were unchanged after the somatostatin infusion. These results suggest that hyperinsulinaemia could help sustain the blood pressure rise in obesity.
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PMID:Reduction of blood pressure in obese hyperinsulinaemic hypertensive patients during somatostatin infusion. 257 63

The cardiovascular, biochemical and hormonal responses to a standard test meal have been investigated in patients with chronic autonomic failure and normal subjects. In autonomic failure there was a rapid (within 15 min), substantial and prolonged fall in blood pressure after the meal. A marked fall in blood pressure also occurred after a liquid meal of similar composition and caloric content, with no change in blood pressure in age-matched subjects with normal autonomic function. In autonomic failure after the test meal the blood pressure reached its nadir (45% fall) after 60 min, and had not returned to pre-meal levels after 3 h. There were no changes in cutaneous and forearm blood flow. In the normal subjects there were no changes in blood pressure after the meal; forearm blood flow fell and cardiac output increased. In autonomic failure there were no changes in plasma noradrenaline levels, unlike the normal subjects. Plasma adrenaline levels were unchanged in both groups. There was a similar rise in levels of plasma renin activity in both groups. The haematocrit and plasma osmolality did not change in either group. Changes in plasma glucose and plasma insulin levels were similar in both groups. The responses of 3 pancreatic gut peptides, neurotensin, pancreatic polypeptide and enteroglucagon, were greater in autonomic failure. Basal levels and responses of vasoactive intestinal polypeptide, cholecystokinin-8 and somatostatin were similar in both groups. The motilin response was greater in normal subjects. We conclude that in patients with autonomic failure there was a rapid, substantial and prolonged fall in blood pressure after a meal. This reduction in blood pressure was not counteracted by an increase in sympathetic nervous activity and other compensatory changes, as occur normally. It was unlikely that osmotic effects of the meal or gut secretions resulted in a significant loss of intravascular fluid into the gut. The fall in blood pressure probably results from vasodilatation within the splanchnic circulation, to which pancreatic and gastrointestinal hormones with vasodilatory actions may contribute.
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PMID:Cardiovascular, biochemical and hormonal changes during food-induced hypotension in chronic autonomic failure. 269 19

Chronic somatostatin administration was found to partially reverse the ACTH-enhanced growth of the rat zona glomerulosa. The effect of somatostatin was completely superposable to that of captopril, a specific inhibitor of the angiotensin-converting enzyme, and the inhibitory actions of these two agents did not cumulate. Neither somatostatin nor captopril counteracted the ACTH-induced stimulation of the growth and steroidogenic capacity of the rat zona fasciculata. These findings support the view that somatostatin acts as an exclusive and specific modulator of the adrenoglomerulotrophic action of the renin-angiotensin system.
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PMID:Further studies on the inhibitory effects of somatostatin on the growth and steroidogenic capacity of rat adrenal zona glomerulosa. 287 79

The study was conducted to examine the effect of somatostatin on activated renin-angiotensin-aldosterone system in a case of Bartter's syndrome. After 60 minutes of 500 micrograms of somatostatin infusion, the plasma aldosterone concentration was reduced from the basal level of 250 pg/ml to 140 pg/ml, whereas plasma renin activity remained at the basal level. This result suggests that somatostatin may specifically inhibit aldosterone secretion in Bartter's syndrome and the agent can be applied to a treatment of this syndrome.
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PMID:Somatostatin suppresses plasma aldosterone concentration in a case of Bartter's syndrome. 288 25

The effects of a new somatostatin analogue SMS 201-995 (H-D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr(ol), Sandostatin) on the orthostatic stimulation of plasma renin activity (PRA) following head-up tilting and on angiotensin II (Ang-II) induced aldosterone (PA) release were studied under placebo controlled conditions in separate groups of healthy volunteers consisting of six and 10 subjects, respectively. Head-up tilting (by 60 degrees) produced the characteristic increases in PRA and PA. Administration of SMS 201-995 significantly (P less than 0.05) inhibited this PRA elevation from 30 min on. Throughout the study period, PA levels were not consistently altered by this analogue. Furthermore, SMS 201-995 failed to inhibit the stimulation of PA secretion induced by exogenous angiotensin-II (2-10 ng/kg/min). Results presented here are at variance with data collected with natural somatostatin showing an inhibitory effect on stimulated PA. This discrepancy can be explained by the recently described absence of SMS 201-995 binding sites in primate adrenal cortex and in human aldosteronomas.
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PMID:Effect of a new somatostatin analogue SMS 201-995 (Sandostatin) on the renin-aldosterone axis. 304 92


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