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)

Using a new in vitro procedure of the isolated perfused rat pancreas with vagal innervation, electrical vagal stimulation produced an increase in both insulin and glucagon secretion in proportion to the pulse frequency, but an inhibition in somatostatin release. When atropine was infused, both insulin and glucagon responses to vagal stimulation were partially suppressed, whereas somatostatin release was enhanced. In the presence of hexamethonium, vagal stimulation failed to affect insulin, glucagon, or somatostatin secretion. Propranolol partially blocked both insulin and glucagon responses but did not influence somatostatin response. Phentolamine had no significant effect on release of hormones. Simultaneous administration of propranolol and phentolamine tended to inhibit both insulin and glucagon responses to vagal stimulation. These findings suggest that not only a cholinergic but also a noncholinergic neuron may be involved in vagal regulation of pancreatic hormone secretion and that these neurons may be under the control of preganglionic vagal fibers via nicotinic receptors.
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PMID:Vagal regulation of insulin, glucagon, and somatostatin secretion in vitro in the rat. 288 48

1. The effects of continuous stimulation of the peripheral end of the ascending cervical sympathetic nerve were compared with those of intermittent stimulation, so arranged as to deliver the same total number of impulses, in cats under chloralose anaesthesia. 2. Continuous stimulation caused a flow of saliva at 5-10 Hz, but not at 2 Hz. In contrast, the same total number of impulses delivered intermittently in bursts elicited a prompt secretion at a frequency as low as 20 Hz for 1 s at 10 s intervals (corresponding to 2 Hz continuously) and a significantly higher rate of secretion at 50 Hz in bursts than that obtained in response to 5 Hz continuously. 3. Continuous stimulation also caused a rise in submandibular vascular resistance (s.v.r.), which persisted throughout the period of stimulation, and was followed immediately thereafter by an intense but transient fall in s.v.r. During stimulation in 1 s bursts, each burst was followed first by a brief rise in s.v.r. and shortly after by a fall. The balance between these two components varied widely between individual animals but often led to an overall fall in s.v.r. during stimulation i.e. complete reversal of the mean vascular effect. A further fall in s.v.r. was then recorded when the stimulus was discontinued. 4. Propranolol (1.0 mg/kg) reduced but failed to abolish the secretory response. It also altered the balance between the two phases of the vascular response slightly in favour of a rise in s.v.r. during stimulation, without apparently affecting the size of the after-dilatation. 5. Pre-treatment with dihydroergotamine (1.0 mg/kg) invariably blocked secretion and revealed a small vasodilator response during sympathetic stimulation with either pattern of stimulation; it also blocked the after-dilatation. 6. Following combined pre-treatment with propranolol and dihydroergotamine, to produce total adrenergic blockade, there was a small residual vasoconstrictor component which amounted to an increase in mean s.v.r. of about 20% during stimulation at 10 Hz continuously. This may have been due to release of neuropeptide Y (NPY). 7. Small but significantly greater amounts of NPY were released into the effluent blood during stimulation of the ascending cervical sympathetic nerve at 70 Hz in bursts than during continuous stimulation. No significant release of vasoactive intestinal peptide (VIP), somatostatin, bombesin, substance P or calcitonin gene-related peptide (CGRP) was observed during stimulation at any frequency.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of stimulating the sympathetic innervation in bursts on submandibular vascular and secretory function in cats. 289 12

The effects of somatostatin on lateral hypothalamic self-stimulation were investigated in rats pretreated with haloperidol, bicuculline, phenoxybenzamine or propranolol. Somatostatin decreased the rate of self-stimulation. Halperidol, bicuculline and phenoxybenzamine potentiated the somatostatin-induced depression of self-stimulation behaviour. Propranolol had no effect. It is suggested that dopaminergic, GABAergic and noradrenergic systems are involved in the somatostatin-induced depression of self-stimulation.
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PMID:Effects of somatostatin on self-stimulation behaviour in rats pretreated with a receptor blocker. 289 12

1. The development of post-exercise ketosis is not abolished by the ingestion of glucose immediately after exercise, despite inducing high insulin/glucagon ratios in the peripheral (and therefore by implication in the portal) blood. 2. To investigate the possibility of autonomic control of the liver influencing its sensitivity to the major counter-regulatory hormones, we administered 50 g glucose, either on its own, or together with 0.5 mg prazosine, 40 mg propranolol, or 15 mg propantheline, to forty-seven 48 h carbohydrate-starved athletes who had just run 25 km. 3. The blood 3-hydroxybutyrate concentration rose from 0.30 +/- 0.05 (mean +/- S.E. of mean) to 0.52 +/- 0.08 mmol/l with exercise, and then to 1.32 +/- 0.40 mmol/l at 6 h after exercise in subjects who had ingested only glucose after exercise. 4. The effects of prazosine and propantheline on the blood ketone body concentration at 2 h after exercise was not statistically significant. Propranolol, on the other hand, significantly lowered the blood 3-hydroxybutyrate concentration (compared with controls) to 0.09 +/- 0.03 mmol/l at 3 h (P less than 0.01), and 0.35 +/- 0.08 mmol/l at 6 h (P less than 0.01) after exercise. 5. The plasma insulin, glucagon, glucose and free fatty acid concentrations were unaffected by propranolol, indicating that the antiketogenesis was the result of a direct effect on ketone body metabolism. 6. Since beta-adrenergic blockade has not previously been shown to have antiketogenic activity, except in somatostatin-induced hyperketonaemia, it is concluded that its effectiveness in post-exercise ketosis can probably be ascribed to a functional hepatic insulin and glucagon deficiency.
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PMID:Beta-adrenergic blockade restores glucose's antiketogenic activity after exercise in carbohydrate-depleted athletes. 331 99

This study was conducted to characterize the mechanisms of hyperglycaemia in exercising sheep. Sheep were run on a treadmill for 45 min (5.5 km h-1, 8% incline) during adrenergic blockade (propranolol or phentolamine mesylate infusions) and during suppression of the rise in glucagon by infusion of somatostatin (SRIF). Propranolol did not alter the glucagon, insulin or glucose responses, except it tended to increase the metabolic clearance of glucose, presumably as a result of blocking the beta-adrenergic inhibition of glucose uptake. Phentolamine mesylate administration was associated with a suppression of the rise in glucagon concentrations, a reversal of alpha-adrenergic inhibition of insulin release and a reduction in glucose appearance during exercise. SRIF prevented the rise in glucagon and reduced insulin concentrations to below resting values. Propranolol and phentolamine mesylate did not alter the glucagon, insulin or glucose response to SRIF. However, SRIF prevented the insulin rise that occurred during phentolamine administration. The increment in glucose appearance produced in response to exercise was the same for SRIF, plus phentolamine mesylate and phentolamine mesylate in the first 25 min of exercise, but was significantly less than in the controls. During the last 20 min of exercise, glucose appearance was not significantly different from the control for any of the groups. The depression by SRIF and alpha-adrenergic blockade of the increment in glucose appearance due to exercise was associated with an impairment of the glucagon response. It appears, therefore, that glucagon may stimulate glucose production early in exercise in sheep directly, as well as by having a permissive effect.
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PMID:Effects of somatostatin and adrenergic blockade on glucagon, insulin and glucose in exercising sheep. 612 38

The effects of adrenergic stimulation and suppression on somatostatin (SS), insulin, and glucagon release were studied in intact dogs. Isoproterenol, a beta-adrenergic agonist, significantly increased portal venous and arterial levels of SS and arterial levels of insulin and glucagon. Propranolol, a beta-adrenergic antagonist, significantly decreased portal venous SS and suppressed the isoproterenol-stimulated increases in the levels of SS, insulin, and glucagon. alpha-Adrenergic stimulation (propranolol plus epinephrine) decreased portal venous SS and arterial insulin. Phentolamine, and alpha-adrenergic antagonist, increased portal venous and arterial SS and arterial glucagon. These data suggest that in intact dogs, stimulation of beta-adrenergic receptors enhances the release of SS, insulin, and glucagon, while stimulation of alpha-adrenergic receptors inhibits the release of SS and insulin without having a definitive effect on glucagon.
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PMID:Adrenergic control of somatostatin release. 612 51

The effects of alpha-, beta- or alpha + beta-adrenergic blockade on arterial plasma concentrations of insulin, glucagon and somatostatin in response to splanchnic nerve stimulation were studied in anesthetized cats. In control experiments splanchnic nerve stimulation caused a marked rise in plasma glucose and glucagon concentrations and a marked fall in insulin but somatostatin was unaffected. Pretreatment with phentolamine significantly increased basal plasma insulin concentration but the response pattern to splanchnic nerve stimulation was not altered. Propranolol attenuated both the glucose and insulin responses. Combined alpha-and beta-blockade abolished the hyperglycemia and hypoinsulinemia induced by splanchnic nerve stimulation, whereas the rise in plasma glucagon was not affected. It is concluded that insulin release from the pancreas and glucose release from the liver is controlled by adrenergic mechanisms whereas pancreatic glucagon and somatostatin secretion is relatively insensitive to splanchnic nerve stimulation in cats.
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PMID:Effects of adrenergic blockade on the release of insulin, glucagon and somatostatin from the pancreas in response to splanchnic nerve stimulation in cats. 613 9

In the present study the role of beta-receptors in the behavioral action of somatostatin was investigated. Somatostatin inhibited extinction of the active avoidance behavior. Propranolol alone had no action on this behavior but significantly inhibited the peptide-induced effect. In the open-field test somatostatin induced locomotor activation; propranolol did not influence this effect of the peptide. Somatostatin inhibited electroconvulsive shock-induced amnesia. Propranolol alone had no action in this test, but significantly decreased the antiamnesic effect of the peptide. These results suggest that the central beta-receptors play an important role in the behavioral action of somatostatin.
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PMID:The effects of interaction between propranolol and somatostatin on the active avoidance behavior, open-field activity and electroconvulsive shock-induced amnesia of rats. 613 74

In order to determine if a rise of circulating catecholamines occurs during somatostatin (SRIF) infusion in normal man, and if this increase plays a significant metabolic role, we infused four normal subjects with SRIF (500 micrograms/h) alone or associated with either alpha-(phentolamine) or beta-(propranolol) adrenergic blocking agents. During SRIF infusion, the initial small decrease in blood glucose was followed by a rise of epinephrine from 25-46 ng/liter (range) to 117-143 ng/liter (range) (P less than 0.05) at 80 min and norepinephrine from 204 +/- 16 to 418 +/- 60 ng/liter at 90 min (P less than 0.05). Thereafter, plasma nonesterified fatty acids, blood glycerol, and ketone bodies increased significantly. Phentolamine adjunction modified neither the catecholamines rise, nor the metabolic changes. Propranolol adjunction did not modify the glucose fall and the catecholamine rise, but resulted in blunted increments of fatty acids and glycerol and in an almost complete suppression of the increase of ketone bodies. These results suggest that the enhanced lipolysis and ketogenesis observed during SRIF infusion are not only due to the SRIF-induced insulin deficiency but also in part to a beta-receptor mediated effect of catecholamines.
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PMID:Role of catecholamines in the ketonemic response to somatostatin in normal man. 613 24

We studied the autonomic nervous control of pancreatic somatostatin secretion using isolated perfused pig pancreases prepared with either intact vagal or splanchnic nerve supply. Electrical stimulation of the vagus nerves increased pancreatic protein output 59-fold, whereas somatostatin output decreased to 57% of prestimulatory secretion. Acetylcholine mimicked the somatostatin response to vagal stimulation, and atropine abolished the inhibition. Splanchnic nerve stimulation increased perfusion pressure up to threefold, whereas somatostatin output decreased to 68%. Phenoxybenzamine abolished the pressure response to splanchnic nerve stimulation and reversed the inhibition to a 20% increase in somatostatin output. Propranolol did not influence the inhibitory effect of splanchnic stimulation but abolished the increase seen after phenoxybenzamine. It is concluded that both divisions of the autonomic nerve supply to the pancreas are inhibitory to somatostatin secretion, but increased secretion may be brought about by a beta-adrenergic mechanism.
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PMID:Autonomic nervous control of pancreatic somatostatin secretion. 614 Aug 51


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