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)

Growth hormone (GH) secretion is mediated by hypothalamic factors, mainly growth hormone releasing factor (GRF) and somatostatin (SS). The hypothalamic hormones, under direct neurotransmitter control, stimulate GH secretion through different central mechanisms. Atropine, an anticholinergic agent, can cross the blood-brain barrier and inhibit GH secretion stimulated by exercise and sleep in normal persons. In order to study the inhibiting effect of atropine on GH release and whether glucose can be replaced by atropine, normal persons and acromegaly patients were observed during exercise, after atropine, and 100 g glucose loading. The results confirmed that GH secretion increases after exercise and that this GH elevation can be inhibited by atropine in normal subjects. But in acromegaly patients high basal GH levels can not be inhibited by 100 g glucose loading or 0.6 mg atropine during the active phase of the disease. Blood sugar levels remained unchanged during the atropine test. It is suggested that the atropine test can be used as a GH inhibitory test in acromegaly patients with overt diabetes.
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PMID:Inhibitory effects of atropine on growth hormone release in normal subjects and acromegaly. 250 52

Pancreatic hormone release is generally thought to be regulated through adrenergic as well as muscarinic receptors. We have previously observed possible nicotinic involvement in insulin release. In the present study, we incubated isolated rat islets for 60 min with various concentrations of atropine (a muscarinic receptor blocker), alpha-bungarotoxin (alpha-Btx, a nicotinic receptor blocker), and anti-acetylcholine receptor antibody (IgG) (anti-Ach.R.Ab) obtained from a patient with myasthenia gravis. Atropine suppressed insulin release, and alpha-Btx and anti-Ach.R.Ab potentiated it; atropine did not suppress glucagon release, while alpha-Btx and anti-Ach.R.Ab raised it. None of these agents influenced somatostatin release. These observations suggest that muscarinic as well as nicotinic receptors influence insulin release, as nicotinic receptors do glucagon release. Neither nicotinic nor muscarinic receptors seem to regulate somatostatin release.
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PMID:Participation of nicotinic receptor in hormone release from isolated rat islets of Langerhans. 256 21

In monogastric animals, suckling influences the secretion of gastrointestinal hormones during lactation. The aim of the present study was to investigate whether similar effects are induced by milking in cows. Experiments were performed on four cows in midlactation. Blood samples were drawn from a chronic jugular vein catheter and gastrin, and somatostatin were determined by radioimmunoassay. Milking and feeding increased plasma gastrin. Somatostatin increased at morning milking and at feeding, but it decreased at evening milking. Atropine injected subcutaneously 30 min before milking increased resting concentrations of gastrin but decreased resting concentrations of somatostatin. Feeding-induced release of gastrin remained but the milking-induced release disappeared. The milking- and feeding-induced effect on somatostatin became more marked. We suggest that milking influences gastrin and somatostatin via activation of the vagal nerves. The gastrin release caused by milking may be mediated via a cholinergic mechanism, whereas the atropine resistant effect on gastrin caused by feeding and on somatostatin caused by both milking and feeding suggest that a noncholinergic, perhaps peptidergic, transmitter may be involved.
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PMID:Milking and feeding-induced release of the gastrointestinal hormones gastrin and somatostatin in dairy cows. 257 1

The effects of atropine, proglumide, and somatostatin analogue (SMS 201-995) on bombesin-induced gallbladder contraction and plasma cholecystokinin (CCK) secretion were investigated in healthy volunteers. The gallbladder size was measured by real-time ultrasonography and the plasma CCK levels by radioimmunoassay. Bombesin (5 micrograms/30 min infusion) induced gallbladder contractions that reduced the gallbladder area to 36.6 +/- 2.1% of the original area 45 min after bombesin infusion, and caused a significant increase of plasma CCK from a basal level of 10.3 +/- 1.8 pg/ml to a peak level of 42.9 +/- 8.9 pg/ml (p less than 0.01) at 20 min. Atropine (500 micrograms, im) inhibited significantly (p less than 0.01) the gallbladder contraction (maximum contractile rate, 78.7 +/- 6.4%) in response to bombesin without any change of plasma CCK secretion, whereas proglumide (800 mg/day for 3 days, per os) decreased slightly but not significantly the gallbladder contraction, and had no effect on plasma CCK secretion. On the other hand, SMS 201-995 (50 micrograms, sc) almost completely inhibited both bombesin-induced CCK secretion and gallbladder contraction (maximum contractile rate, 93.6 +/- 6.2%). These findings suggest that atropine inhibits bombesin-induced gallbladder contraction, not via suppression of CCK release, but probably by inhibiting cholinergic mechanisms, whereas somatostatin inhibits gallbladder contraction, at least in part, by the suppression of bombesin-stimulated CCK secretion.
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PMID:Effects of atropine, proglumide, and somatostatin analogue (SMS 201-995) on bombesin-induced gallbladder contraction and CCK secretion in humans. 268 38

Various agents used in the practice of anesthesia were applied in fifty five healthy postmenopausal female volunteers in order to investigate their hypothalamo hypophyseal response to these drugs, by measuring PRL and TSH levels in peripheral blood. Selection of volunteers, separation of blood specimens and RIA techniques were performed according to international standards. Our results show that thiopental, ketamine and dehydrobenzperidine increase PRL levels significantly (p less than 0.05-0.0025) while fentanyl and diazepam do not alter basal PRL values (p greater than 0.10). It is assumed that thiopental and ketamine may affect the hypothalamo hypophyseal axis through a cholinergic mechanism, whereas dehydrobenzperidine through a dopaminergic one. Atropine reduces the increase in PRL levels caused by thiopental and ketamine, while it does not affect PRL high levels induced by dehydrobenzperidine. TSH levels remain unaffected by all drugs, though ketamine shows a statistically indicative mild tendency to increase PRL levels (p less than 0.10). The fact that TSH values remain the same may be due either to the slower release of TSH stores, or to the involvement of a somatostatin-related mechanism in addition to the one described herein.
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PMID:Hypothalamohypophyseal response to drugs used in anesthesia. 281 81

The purpose of these studies was to measure circulating gastrin and somatostatin concentrations during sham feeding in humans and to evaluate the effect of two doses of intravenous atropine on circulating concentrations of these peptides. Gastric acid and bicarbonate secretion and pulse rate were also measured. Sham feeding increased plasma gastrin concentrations by approximately 15 pg/ml but had no effect on plasma somatostatin-like immunoreactivity (SLI). A small dose of atropine (5 micrograms/kg) augmented plasma gastrin concentrations during sham feeding significantly (P less than 0.01), but did not affect plasma SLI. Atropine also significantly inhibited gastric acid secretion and gastric bicarbonate secretion (by 62% and 52%, respectively), but pulse rate was not affected. A larger dose of atropine (15 micrograms/kg intravenously) suppressed plasma gastrin concentrations significantly compared to the smaller 5 micrograms/kg atropine dose (P less than 0.02), so that plasma gastrin concentrations when 15 micrograms/kg atropine was given were not significantly different from those during the control study. 15 micrograms/kg atropine reduced gastric acid and bicarbonate secretion by 81% and 66%, respectively, and also increased pulse rate by 15 min-1. These studies indicate that small doses of atropine enhance vagally mediated gastrin release in humans, probably by blocking a cholinergic inhibitory pathway for gastrin release. Although the nature of this cholinergic inhibitory mechanism is unclear, we found no evidence to incriminate somatostatin. Our finding that the larger dose of atropine reduced serum gastrin concentrations compared with the smaller dose suggests that certain vagal-cholinergic pathways may facilitate gastrin release.
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PMID:Effect of atropine on plasma gastrin and somatostatin concentrations during sham feeding in man. 286 96

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

Recently, data have been presented showing that muscarinic cholinergic agonists or antagonists can modulate, in opposite ways, GH-releasing hormone GHRH)-induced GH release in man. The aim of the present study was, first, to confirm these findings in the rat and, secondly, if confirmed, to investigate the mechanism(s) subserving the effect of cholinergic drugs. In adult male rats bearing chronic indwelling atrial cannulae, pretreatment with the cholinergic antagonists pirenzepine (0.5 mg/kg, i.v.) or atropine (0.5 mg/kg, i.v.) significantly reduced the rise in plasma GH induced by GHRH (2 micrograms/kg, i.v.), while pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) potentiated it. In rats with hypothalamic somatostatin (SRIF) depletion, i.e. rats with anterolateral deafferentation of the mediobasal hypothalamus or rats treated with cysteamine, the modulatory action of cholinergic drugs on the neuroendocrine effect of GHRH was completely lacking. In these two experimental models, an antiserum raised against SRIF failed to elicit a rise in plasma GH and measurement of hypothalamic SRIF content revealed a clear-cut reduction of the neuropeptide. Atropine (1 mumol/l) and pilocarpine (1 mumol/l), added to pituitary cells in vitro, failed to alter GHRH-induced GH release. The present results indicate that muscarinic cholinergic agonists and antagonists modulate GHRH-induced GH release in the rat and suggest that the effect of cholinergic modulation takes place through SRIF.
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PMID:Cholinergic agonist and antagonist drugs modulate the growth hormone response to growth hormone-releasing hormone in the rat: evidence for mediation by somatostatin. 287 63

Carbamoylcholine (carbachol) has been shown to inhibit somatostatin release from gastric D-cells. We observed that this dose-dependent inhibitory effect was accompanied by decreases in cellular cyclic adenosine 3':5'-monophosphate (cAMP) production and increases in parameters of membrane inositol phospholipid turnover. However, after pretreatment of D-cells with pertussis toxin (200 ng/ml), carbachol paradoxically stimulated basal somatostatin release and potentiated the secretagogue action of forskolin. Pertussis toxin pretreatment blocked the ability of carbachol to decrease cAMP production but changes in inositol phospholipid turnover were unaffected. Atropine reversed all of the observed changes induced by carbachol. These data suggest that muscarinic cholinergic receptors mediate both stimulatory and inhibitory regulation of D-cells. The inhibitory effect may involve pertussis toxin-sensitive inhibitory guanine nucleotide binding proteins while the stimulatory effect may result from the consequences of membrane phosphoinositide turnover.
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PMID:Divergent stimulatory and inhibitory actions of carbamoylcholine on gastric D-cells. 288 21

Infusion of the neuropeptide bombesin stimulates the secretion of several gastrointestinal hormones by an unknown mechanism. We have investigated the effects of atropine (15 ng/kg as bolus followed by 2.5 ng/kg X 30 min) and somatostatin (125 micrograms as i.v. bolus followed by 62.5 micrograms/30 min) on the stimulation of 3 hormones (gastrin, cholecystokinin and pancreatic polypeptide) by 60 pmol/kg X 20 min bombesin in 6 healthy volunteers. Plasma samples for measurement of hormones by sensitive and specific radioimmunoassays were obtained at -5, 0, 2.5, 5, 7.5, 10, 15, 20, 25 and 30 min. Bombesin induced significant increases in plasma gastrin (12 +/- 2 to 34 +/- 3 pM; P less than 0.0005), cholecystokinin (1.2 +/- 0.2 to 8.9 +/- 0.7 pM; P less than 0.0001) and pancreatic polypeptide (22 +/- 4 to 72 +/- 19 pM; P less than 0.05). There were great differences between the effects of atropine and somatostatin on the hormonal responses to bombesin. Atropine slightly increased the response of gastrin by 19% and that of cholecystokinin by 15%, but strongly inhibited the bombesin-stimulated pancreatic polypeptide secretion by 97%. On the other hand, somatostatin inhibited the bombesin-induced secretion of gastrin by 48%, cholecystokinin by 82% and pancreatic polypeptide by 107%. These results point to considerable qualitative and quantitative differences in the stimulatory mechanisms of bombesin on the hormones studied.
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PMID:Effect of atropine and somatostatin on bombesin-stimulated plasma gastrin, cholecystokinin and pancreatic polypeptide in man. 288


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