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)

To investigate the effect of vagal nerve stimulation on the release of pancreatic somatostatin, we electrically stimulated (10 Hz, 5 ms, 13.5 mA, and 10 min) the thoracic vagi just below the heart in halothane anesthetized dogs (n = 15). The stimulation increased the pancreatic output of somatostatinlike immunoreactivity (SLI) (delta = +248 +/- 81 fmol/min, P less than 0.005; base-line levels = 455 +/- 150 fmol/min). min). Arterial plasma SLI levels increased as well (delta = +16 +/- 3 fmol/ml, P less than 0.001; base-line levels = 65 +/- 3 fmol/ml), reflecting stimulation of extrapancreatic SLI secretion. Significant vagal activation was verified by a fivefold increase of pancreatic output of pancreatic polypeptide (PP) (delta = +31.4 +/- 5.9 ng/min, P less than 0.001; base-line levels = 7.8 +/- 0.9 ng/min). Atropine pretreatment (n = 6) inhibited partially both the PP response (delta = +7.9 +/- 3.8 ng/min after atropine) and the pancreatic SLI response (delta = +92 +/- 29 fmol/min) to vagal nerve stimulation. However, atropine pretreatment did not modify the arterial SLI response (delta = +20 +/- 7 fmol/ml). Hexamethonium pretreatment (n = 9) completely abolished all three responses. We conclude that 1) electrical stimulation of the vagus stimulates pancreatic SLI, extrapancreatic SLI, and PP release in vivo in the dog; 2) both muscarinic and nonmuscarinic mechanisms mediate the PP and pancreatic SLI responses; 3) a nonmuscarinic mechanism mediates the extrapancreatic SLI response; and 4) all three responses are mediated via ganglionic nicotinic receptors.
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PMID:Effect and mechanism of vagal nerve stimulation on somatostatin secretion in dogs. 286 92

Addition of gamma-aminobutyric acid (GABA) to antral mucosal fragments in short-term incubation results in dose-dependent and bicuculline-sensitive stimulation of gastrin release and inhibition of somatostatin release, respectively. These effects of GABA on antral gastrin and somatostatin release closely resembled the actions of cholinergic agonists on G- and D-cell function. The present study examines the possibility that the effects of GABA on antral peptide release may be mediated, in part, through stimulation of antral cholinergic neurons. Inclusion of either atropine or pirenzepine in incubation medium prevented GABA-induced stimulation of gastrin release and inhibition of somatostatin release. Addition of the acetylcholinesterase inhibitor, physostigmine, caused a leftward shift in the GABA dose-response curve and increased by 10-fold the sensitivity of the antral preparation to GABA stimulation. Studies with tetrodotoxin suggest that GABA-stimulated gastrin release is mediated through activation of neurons contained within the antral mucosal/submucosal fragments. Hexamethonium, the ganglionic nicotinic receptor antagonist, did not affect GABA-induced gastrin release. These results indicate that GABA affects antral gastrin and somatostatin release through stimulation of antral postganglionic cholinergic neurons.
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PMID:Cholinergic mediation of gamma-aminobutyric acid-induced gastrin and somatostatin release from rat antrum. 287 17

The patterns of somatostatin secretion from the fundus, the main source of somatostatin, and the antrum, the site of paracrine regulation of gastrin secretion, were examined using perifused antral and fundic segments from rat stomach. Gastrin secretion fundic segments from rat stomach. Gastrin secretion could be obtained from antral segments only. Somatostatin secretion was obtained from both antral and fundic segments. 1,1-Dimethyl-4-phenylpiperazinium (DMPP) (10(-5) and 10(-4) M) and bombesin-14 (10(-8) and 10(-6) M) caused concentration-dependent increases in somatostatin secretion that were of the same magnitude in antral and fundic segments. These increases were also of the same magnitude as those obtained in the vascularly perfused whole stomach. Atropine (3 X 10(-7) M) inhibited the somatostatin response to DMPP (10(-4) M) to the same extent in antral (50 +/- 12% inhibition) and fundic (55 +/- 12% inhibition) segments. Hexamethonium (10(-5) M) also inhibited the response to DMPP to the same extent in antral (80 +/- 9%) and fundic (78 +/- 19%) segments. Methacholine caused a typically muscarinic decrease in somatostatin secretion that was of the same magnitude in antral (27 +/- 6%) and fundic (25 +/- 6%) segments. The identical patterns of somatostatin secretion from the two regions of the stomach imply that somatostatin secretion measured in the vascularly perfused whole stomach is a valid reflection of somatostatin secretion by the antrum.
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PMID:Identical patterns of somatostatin secretion from isolated antrum and fundus of rat stomach. 289 24

In cats electrical vagal stimulation leads to an atropine-resistant release of gastrin. Hexamethonium on the other hand blocks the release response. These data suggest that at least one noncholinergic and one cholinergic neuron are involved in the vagal pathway innervating the gastrin producing cells. Exogenously administrated somatostatin also inhibits the vagally induced release of gastrin. Vagal stimulation decreases the levels of somatostatin in portal blood, suggesting that a release of gastric somatostatin, occurring during basal conditions, is inhibited. It is therefore possible that the vagally induced release of gastrin is in part secondary to the decreased somatostatin secretion. In contrast, electrical stimulation stimulates the release of gastrin as well as that of somatostatin into the antral lumen. However, the intraluminal release of these peptides only occurs in the presence of low antral pH. In rats, low doses of atropine (0.05 mg/kg) completely inhibits the intragastric vagally mediated release of somatostatin, which leads to an approximately 10-fold enhancement of the simultaneously occurring gastrin release. The intraluminally released somatostatin most likely derives from pH sensitive antral D cells of the open type. The vagal innervation of this population of somatostatin producing cells appears to be cholinergic. Activation of the sympathetic nervous system inhibits the vagally induced release of gastrin dependently of the prevailing antral pH. This inhibitory effect is probably exerted by a neurogenic mechanism at the ganglionic level. In contrast, basal gastrin release is enhanced by activation by the sympathoadrenal system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurogenic control of release of gastrin and somatostatin. 614 89

The effects of atropine and hexamethonium on submandibular vasodilation, secretion and VIP release in response to parasympathetic nerve stimulation were studied in cats. It was found that salivary secretion was completely atropine sensitive at all frequencies. The vasodilatory response was characterized by an initial phase (most marked at lower frequencies) followed by a maintained phase (most pronounced at high frequencies). Atropine reduced the initial phase at all frequencies while the maintained phase was reduced only at low stimulation frequencies. At 15 Hz the maintained blood flow response was paradoxically increased after atropine, particularly with regard to the duration. The increase in blood flow after atropine was accompanied by an about eight fold increase in VIP output as compared to control stimulations at 15 Hz. This may suggest that the acetylcholine levels regulate the VIP release in a feed-back system via muscarinic autoreceptors. No increase in VIP output by atropine was, however, observed at 2 Hz while a small but significant increase was found at 6 Hz. Treatment with VIP antiserum reduced both phases of the vasodilation as well as the secretion in response to stimulation at 2 Hz. Thus, VIP and acetylcholine seem to be important for both phases of vasodilation as well as for salivary secretion. The relative contributions of VIP and acetylcholine are, however, hard to evaluate since atropine appears to increase VIP release. This fact complicates the characterization of cholinergic and noncholinergic vasodilator mechanisms by the use of atropine. Hexamethonium treatment abolished both the vasodilation, the secretion and the VIP release seen during parasympathetic nerve stimulation implying that it was preganglionic and that the preganglionic transmitter is acetylcholine which activates postganglionic transmitter is acetylcholine which activates postganglionic neurons via nicotinic receptors. Somatostatin had no blocking effect on parasympathetic mechanisms in the cat submandibular gland.
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PMID:Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion. II. Effects of cholinergic antagonists and VIP antiserum. 734 99

The possible involvement of central noradrenergic and/or adrenergic circuits in central mechanisms controlling free fatty acids and glucose levels was investigated in conscious pigeons. The effects of intracerebroventricular injections of noradrenaline (80 nmol) or adrenaline (80 nmol) on plasma free fatty acids and glucose concentrations were examined. The possible role of the autonomic nervous system, of sympathetic terminals and of pituitary hormone release in the metabolic responses induced by intracerebroventricular injections of adrenaline and noradrenaline was investigated by systemic pretreatment with a ganglionic blocker (hexamethonium, 1 mg/100 g), guanethidine (5 mg/100 g), and somatostatin (15 microg/100 g), respectively, 15 min before intracerebroventricular administration of adrenaline, noradrenaline or vehicle. Intracerebroventricular noradrenaline injections strongly increased plasma free fatty acid concentration but evoked no change in blood glucose levels, while adrenaline treatment increased glycemia without affecting free fatty acid levels. Hexamethonium did not block the increase in plasma free fatty acids induced by noradrenaline, while somatostatin pretreatment abolished noradrenaline-induced lipolysis during the experimental period. Adrenaline-induced hyperglycemia was blocked by systemic injections of somatostatin, hexamethonium and guanethidine. The present results suggest that: (1) adrenergic and noradrenergic mechanisms may participate in central control of blood glucose and free fatty acids, respectively, as observed in mammals. (2) noradrenaline-induced lipolysis may be mediated by pituitary mechanisms, and (3) postganglionic sympathetic fibers, possibly innervating the endocrine pancreas, may be involved in adrenaline-induced hyperglycemia.
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PMID:Central injections of noradrenaline and adrenaline differentially affect plasma free fatty acid and glucose in conscious pigeons (Columba livia). 1108 20