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 effects of intracerebroventricular or intracarotid injection of synthetic rat calcitonin gene-related peptide (CGRP) on growth hormone (GH) secretion induced by various stimuli in male rats were examined. CGRP (2.5 or 5 micrograms/rat intracerebroventricularly, i.c.v.) was administered 10 min before beta-endorphin (0.5 microgram/rat i.c.v.) or morphine (1 mg/kg intracarotidly, i.a.) or clonidine (0.25 mg/kg i.a.) or GH-releasing hormone (GHRH1-40; 2 micrograms/kg i.a.). When injected peripherally, CGRP (10 micrograms/rat, i.a.) was administered 5 min before morphine or GHRH. To investigate the possible involvement of somatostatin (SRIF) in the inhibition of GH secretion by CGRP, the effect of the peptide on GHRH-induced GH release was also examined in rats with hypothalamic SRIF depletion obtained by pretreatment (4 h before) with cysteamine (300 mg/kg subcutaneously). Blood samples for hormone determination were drawn from freely moving rats at various times before and after drug treatment. The intracerebroventricular administration of CGRP (5 micrograms/rat) significantly inhibited GH secretion induced by all the stimuli used. In rats with SRIF depletion CGRP did not modify the stimulation of GH by GHRH. When CGRP was administered intracarotidly, even the dose of 10 micrograms/rat did not reduce the GH release induced by GHRH or morphine. The effects of intracerebroventricular CGRP on basal or beta-endorphin-induced prolactin release were also examined. When given intracerebroventricularly, the peptide did not modify prolactin secretion. The present results indicate that CGRP has a central inhibitory role in the control of GH secretion, probably through a stimulation of SRIF release.
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PMID:Evidence of a central inhibition of growth hormone secretion by calcitonin gene-related peptide. 278 61

The function of clonal insulin-secreting RINm5F cells was compared with parent tumoural B-cells from radiation-induced NEDH rat insulinoma and a RINm5Fr cell line established following transplantation of RINm5F cells in NEDH rat. After 3 days culture, tumoural B-cells contained 156 micrograms insulin/10(6) cells and released 57-82 ng insulin/10(6) cells/h during acute incubations at 2.6 mM Ca2+. RINm5F cells contained 0.56 ng insulin/10(6) cells and released 62-181 pg insulin/10(6) cells/h. Unlike tumoural B-cells, secretion was stimulated 1.7-2.4-fold by 5 mM theophylline, 1 microM glucagon, 25 mM K+, or 7.6 mM Ca2+. Subscapular transplantation of cultured tumoural B-cells or RINm5F cells (2.8 X 10(7) cells/rat) resulted in an encapsulated tumour associated with progressive hyperinsulinaemia, hypoglycaemia and death by 28-46 days and 39-44 days respectively. A RINm5Fr cell line was established in culture from a 19 g tumour 20 days after transplantation. RINm5Fr cells contained 2.69 ng insulin/10(6) cells and released 385-1,017 pg insulin/10(6) cells/h (p less than 0.001 compared with RINm5F cells). Secretion was not augmented by glucose, but at 16.7 mM glucose it was stimulated 1.5-fold by 5 mM theophylline, 1.6-fold by 1 microM glucagon and inhibited 0.6-fold by somatostatin. At 5.6 mM glucose, secretion was stimulated 1.6-fold by 25 mM K+, 2.5-fold by 7.8 mM Ca2+, 2.1-fold by 20 microM A23187, 1.5-fold by 20 mM leucine and 1.4-fold by 100 microM tolbutamide. These data indicate fundamental differences between rat insulinoma cells and the derived RIN cell lines. Transplantation is a useful means to enhance the function of RINm5F cells.
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PMID:Insulin secretion in vivo and in vitro from transplantable NEDH rat insulinoma and derived clonal RINm5F cell line. 282 34

Intracerebroventricular (icv) injection of DN1417 (0.3, 3 and 30 nmol/rat), a TRH analog, resulted in a dose-related increase in plasma glucose, epinephrine and norepinephrine levels in conscious male rats. The effects of DN1417 were more potent and longer-lasting than those of TRH on a molar basis. Intravenous injection of DN1417 (30 nmol/rat) did not change plasma glucose, epinephrine and norepinephrine levels. Pretreatment with hexamethonium (1.5 mg/100 g body wt, iv, 2 min before) inhibited plasma glucose, epinephrine and norepinephrine responses to DN1417 (3 nmol/rat, icv). DN1417 did not change plasma glucose, epinephrine and norepinephrine levels in rats after total adrenalectomy. In the animals pretreated with cysteamine (30 mg/100 g body wt, sc, 4 h before), basal plasma glucose, epinephrine and norepinephrine levels were raised, and exaggerated responses of plasma glucose, epinephrine and norepinephrine to DN1417 (3 nmol/rat, icv) were obtained. These results indicate that DN1417 has a potent and long-lasting effect in the central nervous system in stimulating the secretion of catecholamines through the autonomic nervous system, which is associated with an elevation of plasma glucose and that endogenous hypothalamic somatostatin may inhibit the action of DN1417.
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PMID:Central effects of DN1417, a novel TRH analog, on plasma glucose and catecholamines in conscious rats. 285 99

Somatostatin (S) inhibits hemorrhagic gastric erosions produced by ethanol. In this study we compared the dose-dependent effects of linear (reduced) and cyclic (oxidized) S with respect to mast cell degranulation. The gastric mucosal injuries were more inhibited by linear S than by cyclic S. But linear S aggravated injury at a certain dose (10(-7) mol/rat). Mucosal mast cell degranulation correlated significantly with the area of hemorrhagic mucosal lesions (r = 0.91). Both cytoprotection as well as aggravation potency of S may be connected to gastric mucosal mast cell activity in the rat.
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PMID:Effects of somatostatin on ethanol-induced gastric erosions in the rat: role of mast cells. 287 24

Somatostatin and somatostatin derivatives were tested for their ability to prevent gastric hemorrhagic erosions induced by ethanol. The somatostatin analogues were cyclohexapeptides with the rearranged amino acids 7-14 of somatostatin (S-14): Phe-Thr-Lys(Z)-Trp-Phe-D-Pro(I), Phe-Thr-Lys-Trp-Phe-D-Pro(II), Phe-Thr-Lys-D-Trp-Phe-Tyr(III) and Tyr-Phe-D-Trp-Lys-Thr-Phe(IV). In Spraque-Dawley rats receiving ethanol alone, the lesions involved 18.1 +/- 3.2% of the glandular stomach while after S- 14 (10(-7) mol/rat) the lesioned area was reduced to 6.3 +/- 1.1% (p less than 0.05). Peptide I and peptide II (doses 10(-7) -10(-9) mol/rat) decreased the area of erosions to less than 5%. Peptide III was less active and peptide IV was inactive. In rats with chronic gastric fistula S- 14 and peptide II decreased the cysteamine-stimulated acid secretion without affecting the pepsin output. We also continuously measured the intraluminal pH in the stomach of Wistar rats which develop gastric erosions after subcutaneous injection of cysteamine. The erosions were reduced by S- 14 or SMS while the intraluminal pH did not change under the influence of cysteamine or the combination of cysteamine plus S- 14 or SMS. Thus some of the peptides derived from S- 14 exert prominent gastric mucosal protection without influencing gastric secretion.
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PMID:Gastric mucosal protection by somatostatins. 288 58

The effect on prolactin (PRL) secretion of acute administration of new octapeptide analogs of somatostatin (SS) with an enhanced and prolonged growth hormone inhibitory activity was investigated in rats under various pretreatment conditions with estrogen and antidopaminergic drugs. Analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), at a dose of 5 micrograms/100 g body wt, did not decrease basal PRL levels in thiopental-anesthetized female rats, untreated or treated with estrogen benzoate (EB) (8 micrograms/rat) for 5 days. When haloperidol was used to elevate PRL level, a single injection of RC-121 inhibited PRL release in EB-pretreated female rats or untreated female and male rats. Analog D-Phe-Cys-Trp-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160), which has a potency similar to RC-121 in the tests on inhibition of GH, in a dose of 0.2 microgram/100 g body wt, did not lower the elevated PRL level induced by alpha-methyl-p-tyrosine and/or pretreatment with EB (100 micrograms/rat, 3 and 6 days before) in pentobarbital-anesthetized male rats. However, both analogs RC-121 and RC-160, in doses of 0.2 microgram/100 g body wt, decreased the PRL levels elevated by prolonged pretreatment with EB (100 micrograms/rat, twice a week for 3 weeks) in male rats. These results indicate that acute administration of these SS analogs can induce a prolonged inhibition of PRL release when PRL is acutely elevated by haloperidol or chronically elevated by 3 weeks of estrogen administration. Future additional studies are required to investigate the effects of chronic administration of these SS analogs on PRL levels.
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PMID:Inhibitory effects of somatostatin analogs on prolactin secretion in rats pretreated with estrogen or haloperidol. 288 61

Biological activities of highly potent octapeptide analogs of somatostatin (SS), D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), were investigated in male rats. When analog RC-160 was administered to rats in which serum growth hormone (GH) levels were elevated by pentobarbital anesthesia, a dose-related inhibition of GH was obtained at dose range of 0.1 to 2.5 micrograms/kg. The time course of GH inhibition by RC-160, RC-121 and SS-14 was studied in rats treated with phenobarbital, morphine and chlorpromazine. Analogs RC-160 and RC-121 induced a prolonged inhibition of GH levels, in contrast to SS-14, whose effect was short-lived. The analogs suppressed the GH level for more than 2 hr, the peak inhibition being seen 30 to 60 min after the injection. The effects of analogs RC-160 and RC-121 on insulin secretion were observed in rats, in which insulin levels had been elevated by intravenous administration of glucose (500 mg/rat). Administration of RC-160 suppressed insulin secretion, dose-dependently, maximum but not complete inhibition being achieved at a dose of 100 micrograms/kg. In this model, RC-160 and RC-121, in doses of 30 micrograms/kg, induced a similar inhibition of insulin release as 200 micrograms/kg of SS-14, whose action of SS-14 was transient. The effect of analog RC-160 on glucagon release was studied in rats with glucagon levels elevated by hypoglycemia. RC-160 suppressed the secretion of glucagon, the inhibition being dose-dependent in the range of 0.1 to 2 micrograms/kg. Doses of 2 and 10 micrograms/kg of this analog completely suppressed the hypoglycemia-induced glucagon release. These results indicate that analogs RC-160 and RC-121 possess prolonged and enhanced biological activities, the former analog showing a high selectivity in inhibiting GH and glucagon release in vivo as compared with that of insulin secretion.
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PMID:Effects of highly potent octapeptide analogs of somatostatin on growth hormone, insulin and glucagon release. 288 86

The involvement of the cholinergic system in GH secretion has recently acquired increasing importance. Data have been presented suggesting that in rats the effect of cholinergic modulation on GH secretion takes place through inhibition or stimulation of hypothalamic somatostatin (SRIF) release. To investigate further the significance of cholinergic-SRIF link and its role in the regulation of GH secretion, the action of cholinergic agonist and antagonist drugs in the GH short-loop feedback mechanism mediated by SRIF was investigated. Intracerebroventricular (i.c.v.) infusion of 0.2 or 2.0 micrograms GH/rat into the lateral brain ventricle of adult male rats induced a significant reduction in the GH-releasing hormone (GHRH; 2 micrograms/kg, i.v.)-induced peak GH rise, but only the 2.0 micrograms dose reduced also the GH-integrated area after administration of GHRH. This effect was absent after central administration of 20.0 micrograms GH/rat, due probably to leakage of some GH from the cerebral ventricle into the systemic circulation. Pretreatment with cysteamine (300 mg/kg, s.c.), a known depletor of hypothalamic SRIF, or with anti-SRIF serum (0.5 ml/rat) completely counteracted the lessening of the GH response to GHRH induced by 2.0 micrograms GH injected i.c.v. Similarly, pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) completely antagonized the inhibitory effect of central infusion of GH on the GHRH-induced GH response. Atropine (1.0 mg/kg, i.v.), a muscarinic cholinergic antagonist, strikingly inhibited the GHRH-induced GH rise, but when given in combination with i.c.v. infusion of GH there was no additive inhibitory effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Involvement of the somatostatin and cholinergic systems in the mechanism of growth hormone autofeedback regulation in the rat. 289 96

We have studied the rebound secretion of GH following short-term somatostatin (SS) infusions in conscious rats, using an automatic sampling system for withdrawing frequent microsamples of blood. Intravenous infusions of SS (5-50 micrograms/h per rat) inhibited spontaneous GH secretion, but when SS was withdrawn there was a large burst of rebound GH secretion. A sub-anaesthetic dose of urethane reduced such rebound bursts of GH, suggesting a hypothalamic involvement in rebound GH secretion. Passive immunization with an antibody against rat GH-releasing factor (GRF) attenuated the rebound GH secretory response to the withdrawal of an SS infusion (GH concentration during rebound secretion was 26 +/- 21 micrograms/l vs 475 +/- 127 micrograms/l (mean +/- S.E.M.), after 0.5 ml anti-GRF serum or non-immune serum respectively). The inhibition of GH rebound secretion was related to the dose of anti-GRF serum administered. Intravenous infusions of human GH (20-100 micrograms/h per rat) also reduced the size of the rebound GH secretion following SS withdrawal, in both male and female rats. We suggest that the rebound GH secretion that follows SS withdrawal in vivo is caused mainly by a hypothalamic release of GRF. Exogenous GH inhibits SS-induced rebound GH secretion in the conscious rat, possibly by inhibiting hypothalamic GRF release.
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PMID:The rebound release of growth hormone (GH) following somatostatin infusion in rats involves hypothalamic GH-releasing factor release. 290 83

Intracerebroventricular (icv) injection of alpha-human atrial natriuretic polypeptide (alpha hANP) or alpha-rat ANP (0.6 and 3 nmol/rat) elicited an increase in plasma GH levels both in conscious freely moving rats and in urethane-anesthetized rats when given at the trough of spontaneous GH secretion. Antiserum specific for rat GRF did not affect the plasma GH increase induced by icv injection of alpha hANP. Intracerebroventricular injection of alpha ANP (3 nmol/rat) failed to stimulate GH secretion in conscious rats pretreated with cysteamine (30 mg/100 g BW, sc), a depletor of somatostatin (SRIF), and in conscious rats during constant iv infusion of SRIF (55 ng/ml). GH release induced by iv injection of synthetic rat GRF (200 ng/100 g BW) was exaggerated by alpha hANP (3 nmol/rat, icv) in conscious rats. These results suggest that central ANP stimulates pituitary GH secretion possibly by inhibiting SRIF release from the hypothalamus in the rat.
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PMID:Stimulation of growth hormone secretion by central administration of atrial natriuretic polypeptide in the rat. 296 63


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