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)

Rat anterior pituitaries were incubated over a 3-h period. Both PGE2 and GH were increased by GRF in a concentration-related manner (ED50: 3.5 nM and 6.5 nM, respectively). A significant correlation (r = 0.88, n = 127) was observed between GH and PGE2 release over the range of GRF concentrations tested. Among the five prostanoids analyzed, only PGE2 was selectively increased. Somatostatin lowered GH release, without any effect on PGE2 production. Indomethacin (Id) and Aspirin reduced significantly PGE2 synthesis and GRF-induced GH release. The inhibitory effect of Id was counteracted by addition of PGE2 to the medium. GRF and PGE2, at maximal concentrations, had a partial additive effect on GH release. The increase in PGE2 production and the reduced GH release in the presence of cyclooxygenase inhibitors suggest that PGE2 is involved in GRF-induced GH release.
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PMID:Growth hormone-releasing factor (GRF) stimulates PGE2 production in rat anterior pituitary. Evidence for a PGE2 involvement in GRF-induced GH release. 285 4

The effect of GRF adenylate cyclase activation was studied in normal human, bovine and rat pituitary tissues. Human GRF (hGRF) activates adenylate cyclase in normal human pituitary membrane preparations in a concentration dependent manner (ED5 0 = 10(-11) M). In bovine pituitary cells hGRF stimulates GH secretion into the medium (ED5 0 = 7 X 10(-12) M) and activates adenylate cyclase (ED5 0 = 10(-11) M). In normal rat pituitary cells in monolayer culture, rat GRF (rGRF) stimulates adenylate cyclase (ED5 0 = 3 X 10(-11) M). In normal human pituitary membrane preparations and in normal rat pituitary cells in culture, somatostatin inhibits GRF-stimulated adenylate cyclase in a non-competitive manner, while it does not affect basal (i.e. non-stimulated) adenylate cyclase levels. VIP, a peptide which is structurally homologous to hGRF and rGRF is a weak GRF-agonist and activates adenylate cyclase in human and rat pituitary preparations at concentrations greater than 10 nM.
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PMID:GRF is a highly potent activator of adenylate cyclase in the normal human, bovine and rat pituitary: interaction with somatostatin. 285 17

GH3 cells were used to study the effect of rat growth hormone-releasing factor on adenylate cyclase activity and its interaction with somatostatin. Rat GRF stimulates adenylate cyclase activity (ED5 0 = 6 X 10(-8) M) and somatostatin-14 inhibits this GRF-stimulated activity in a non-competitive manner without affecting the basal enzyme levels. Inhibition by somatostatin-14 is observed at concentrations as low as 10(-11) M and the half-maximal effect is obtained with 10(-8) M. Somatostatin-28 is more potent than SS-14 and has an ED5 0 of 3 X 10(-11) M. VIP is more active than rat GRF in stimulating adenylate cyclase activation. We conclude that in GH3 cells rat GRF behaves as a partial VIP agonist by interacting with VIP-preferring receptors and its effects are inhibited by somatostatin.
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PMID:Somatostatin inhibits growth hormone-releasing factor-stimulated adenylate cyclase activity in GH, cells. 285 18

The effect of GH-releasing factor(1-44)(GRF) alone, or together with somatostatin (SRIF), dopamine (DA), vasoactive intestinal peptide (VIP) or cycloheximide was studied in a total of ten human somatotrophinomas using a static cell culture system. Growth hormone-releasing factor (2.0 X 10(-8) mol/l) significantly (P less than 0.05) stimulated GH release from nine out of ten tumours over 4-h incubations, and a dose-related effect (2.0 X 10(-10) -2.0 X 10(-8) mol/l) was observed in five tumours thus studied. Repeated GRF (2.0 X 10(-8) mol/l)-mediated GH release was seen during 96% (n = 25) of experiments performed on six tumours over 4 h and up to 27 days in culture. Growth hormone-releasing factor (2.0 X 10(-8) mol/l) also stimulated GH release from five out of seven somatotrophinomas during 60-min incubations. Somatostatin (6.1 X 10(-9) mol/l) completely inhibited GRF-induced GH secretion from four tumours studied over 4 h, but in each case there was significant (P less than 0.05) 'rebound' of GH release from cultures exposed to both GRF and SRIF during a subsequent recovery period. Dopamine suppressed basal GH release from two out of four tumours, but in each case had a greater inhibitory effect on GRF-mediated GH release. Vasoactive intestinal peptide directly stimulated GH release from two out of three tumours, and the effects were additive to maximal stimulatory doses of GRF. Cycloheximide significantly (P less than 0.01) enhanced GRF-stimulated release of GH during a 60-min incubation, but inhibited both basal and GRF-stimulated release over 4 and 8 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of growth hormone-releasing factor (1-44) on growth hormone release from human somatotrophinomas in vitro: interaction with somatostatin, dopamine, vasoactive intestinal peptide and cycloheximide. 285 45

The secretory pattern of GH in the mature rat is sexually differentiated. In male rats GH is secreted in pulses occurring at regular 3- to 4-h intervals. In females the pulses are lower and plasma GH levels between the pulses are higher than in males. The continuous presence of testosterone appears to be necessary to maintain low basal GH levels in adult male rats. Neonatal, but not prepubertal, gonadectomy decreases GH pulse height in adult male rats to female levels. Administration of testosterone neonatally to castrated animals returns GH pulse height to normal suggesting that neonatal testicular androgen secretion is one determinant for GH pulse height in adult male rats. Administration of testosterone neonatally or during adult life to neonatally ovariectomized rats also produces higher GH pulses. In contrast to testosterone, estrogens elevate basal plasma GH levels and suppress the GH pulses under some conditions. Estrogens may stimulate basal GH secretion by acting directly on the pituitary. The physiological significance of the secretory pattern of GH has been investigated in hypophysectomized rats by simulating different plasma patterns of GH. The results suggest that high, infrequent GH pulses with low plasma GH levels in between (i.e. a masculine plasma GH pattern) promotes growth more effectively than an intermediate, rather constant level of plasma GH (i.e. a feminine plasma GH pattern). Since male sex steroids masculinize the secretory pattern of GH and have only minor growth-promoting effects in hypophysectomized animals it appears that the growth promoting effect of androgens is indirect and is due to an altered secretory pattern of GH. Presumably, neonatal androgen secretion stimulates body growth during adult life by irreversibly masculinizing the secretory pattern of GH. In contrast, estrogens appear to influence body growth by mechanisms that are mainly independent of the secretory pattern of GH. Evidence is accumulating that the secretory pattern of GH in the rat also affects various sexually differentiated hepatic characteristics such as steroid metabolism and prolactin receptor concentration. Thus, a feminization of the liver develops after continuous, but not intermittent, administration of GH to hypophysectomized rats. GH secretion is predominantly regulated by two hypothalamic peptides; GRF, and the GH-release-inhibiting factor, somatostatin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sexual dimorphism in the control of growth hormone secretion. 286 Oct 84

The effect of synthetic human GH-releasing factor (hGRF-40) on somatostatin (SRIF) release from the median eminence of the hypothalamus was evaluated in rats with use of an in vitro incubation system. hGRF-40 stimulated SRIF release in a dose-related manner. This effect was significant at concentrations varying from 10(-11)-10(-7) M, with a minimal effective dose of 10(-11) M. Maximal stimulation was observed at 10(-10) M. Pimozide was added in vitro at a concentration of 10(-6) M to block dopamine (DA) receptors, since DA is a known stimulator of SRIF release. Pimozide was without effect on SRIF release and did not alter the stimulatory effect of hGRF-40. To evaluate the possibility that DA and GRF may share a common pathway to stimulate SRIF release, median eminence fragments were simultaneously exposed to submaximal concentrations of both DA (6 X 10(-7) M) and hGRF-40 (10(-12) M). By themselves, each of these doses had little effect on SRIF release. When they were added together, a marked stimulation was noted, which was not, however, significantly greater than the sum of the responses to each agent alone. These results suggest that DA and GRF act by separate mechanisms to stimulate SRIF release. GRF may be physiologically involved in the regulation of SRIF release. Stimulation of SRIF release may be a mechanism by which GRF exerts a negative ultrashort-loop feedback to inhibit GH release.
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PMID:Stimulation of somatostatin release in vitro by synthetic human growth hormone-releasing factor by a nondopaminergic mechanism. 286 13

The effect of ventromedial-arcuate (VMH-ARC) nuclei lesions on plasma growth hormone (GH) response to human growth hormone-releasing factor (GRF, 1 microgram/kg b.wt., i.v.) was studied in conscious rats after they had received chlorpromazine (CPZ) or CPZ plus antiserum against somatostatin (ASS). When rats were pretreated with CPZ alone, there was no difference in basal plasma GH level between VMH-ARC lesioned rats and controls. The magnitude of plasma GH response to GRF in 5 out of 6 VMH-ARC lesioned rats exceeded that of controls. When the same observation was repeated using the same rats after they had received ASS and CPZ, basal plasma GH levels of controls were significantly higher than those of VMH-ARC lesioned rats, and the magnitude of the plasma GH response to GRF was augmented in both groups of rats. The plasma GH response to GRF was comparable between two groups, though the peak plasma GH response to GRF was slightly but significantly lower in VMH-ARC lesioned rats as compared to controls. Pituitary GH content was reduced significantly in VMH-ARC lesioned rats as compared to controls. The results demonstrate that the pituitary responsiveness to GRF does not appear to be altered significantly in rats bearing bilateral VMH-ARC lesions. In addition, the placement of electrolytic lesions in VMH-ARC regions causes reduced SS secretion into the hypophyseal portal vessels and leads to an augmentation of plasma GH response to GRF.
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PMID:Effect of hypothalamic ventromedial lesions on plasma growth hormone response to growth hormone-releasing factor in rats. 286 81

The influence of 4 releasing factors on the release of somatostatin (SRIF) from the median eminence of the hypothalamus in rats was studied using an in vitro system. Synthetic growth hormone-releasing factor (hGRF-40) and corticotropin releasing factor (CRF) stimulated SRIF release, whereas thyrotrophin-releasing hormone (TRH) and luteinizing hormone releasing hormone (LHRH) did not stimulate its release. CRF and GRF may be physiologically involved in the regulation of SRIF release.
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PMID:The influence of hGRF, CRF, TRH and LHRH on SRIF release from median eminence fragments. 286 18

The effect of human GRF 44 upon somatostatin-inhibited pancreatic and gastric secretions was studied in rats with chronic fistulas. GRF did not show any antagonist action of somatostatin on these gastro-intestinal organs. GRF alone had a small inhibitory effect on gastric acid output.
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PMID:Growth-hormone releasing factor does not antagonize somatostatin effects on pancreatic and gastric secretions. 286 10

The effects on islet hormone secretion of the synthetic replicates of two peptides with potent GH-releasing activity isolated from human pancreatic islet cell tumors (GRF-40 and GRF-44) were studied using the isolated, perfused dog pancreas. GRF-40 produced a dose-dependent stimulation of insulin, glucagon, and somatostatin secretion. The responses to GRF-40 were modified by the prevailing glucose level: higher insulin and somatostatin and lower glucagon responses were obtained at high rather than low glucose. In contrast, GRF-44 did not produce any stimulation of the endocrine pancreas. In vivo GRF-40 and GRF-44 elicited identical pronounced growth hormone responses in the rat. The findings reported here provide support that pancreatic insulin and glucagon are modulated by GRF-40 with somatostatin as its inhibitory counterpart. The question, whether GRF-40 is of physiologic relevance in the regulation of the endocrine pancreas, must await evidence that it is present and releasable from the pancreas.
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PMID:Synthetic pancreatic growth hormone-releasing factor (GRF-40) stimulates the secretion of the endocrine pancreas. 286 96


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