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)

Gallbladder mucosal net fluid transport and motility were measured in vivo by a continuous perfusion technique in the anaesthetized cat. Prostaglandin E2, administered to the perfused gallbladder lumen, caused a contraction decreasing gallbladder volume capacity, and induced a secretory response by the mucosa. These effects by prostaglandin E2 were abolished by the nerve-blocking agent tetrodotoxin (administered close intraarterially) and somatostatin (administered intravenously), but not by intravenous hexamethonium. Atropine (administered intravenously) reduced the order of magnitude of the gallbladder contraction in response to prostaglandin E2 but did not affect the secretory response by the mucosa. Neither of these drugs significantly affected gallbladder volume capacity or mucosal fluid transport during basal conditions. Tetrodotoxin did not abolish the gallbladder responses to intravenous cholecystokinin or vasoactive intestinal peptide, peptides known to act directly upon smooth muscle and epithelial cell receptors, respectively. It is suggested that prostaglandin E2 affects gallbladder function in vivo mainly by activation of postganglionic non-cholinergic intramural nerve cells.
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PMID:Intraluminal prostaglandin E2 affects gallbladder function by activation of intramural nerves in the anaesthetized cat. 290 7

We studied in five healthy volunteers whether the cholinergic pathway regulated the secretion of gastric intraluminal somatostatin-like immunoreactivity (SLI) in response to stimuli of pentagastrin infusion (0.9 micrograms/kg/h, intravenously) and sham feeding. We measured gastric secretory volume, hydrogen ion output, and SLI at base line, during pentagastrin infusion, after sham feeding, and after applications of atropine (0.0, 0.7, 7.0 micrograms/kg, intramuscularly) given before pentagastrin and sham feeding. The stimuli were given randomly, at separate times on different days. After each stimulus, eight 15-min gastric juice collections were made; samples were adjusted to pH 7, pepstatin-A and aprotinin were added, and samples were extracted with acetone to determine SLI by radioimmunoassay. Pentagastrin and sham feeding significantly increased gastric luminal SLI secretion, which appeared to correlate with the increases in volume and acid output. Atropine at 7 micrograms/kg significantly suppressed gastric volume, acid, and SLI outputs stimulated by sham feeding; however, responses to pentagastrin stimulation remained unchanged. To conclude, the cholinergic mechanism regulates gastric intraluminal SLI response to sham feeding but not to pentagastrin infusion.
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PMID:Mechanism of release of gastric luminal somatostatin-like immunoreactivity in response to pentagastrin and sham feeding in man. 343 15

The effects of 2-deoxy-D-glucose (2-DG) on plasma levels of somatostatin-like immunoreactivity (SLI) were examined in conscious normal dogs. After an iv infusion of 2-DG (400 mg/kg . h for 15 min), plasma SLI rose significantly from a mean baseline of 130 +/- 5 pg/ml (mean +/- SEM) to a mean peak of 204 +/- 25 pg/ml (P less than 0.005) at 25 min. Plasma insulin and glucagon also increased significantly. Atropine (200 microgram/kg . h for 35 min, iv) and hexamethonium (5 mg/kg, iv) markedly suppressed the SLI response to 2-DG, suggesting that it might be mediated, at least in part, by the autonomic nervous system. In contrast, the plasma insulin and plasma glucagon responses to this glucose analog were only slightly affected by atropine or hexamethonium pretreatment. Carbachol (0.2 mg, sc) caused a mean maximal increase in SLI of 43 +/- 14% (P less than 0.005) and atropine (200 micrograms/kg . h, iv) caused a mean maximal decrease of 25 +/- 2% (P less than 0.001) from the respective baseline levels. Plasma insulin and glucagon rose promptly after carbachol and were unchanged by atropine. To assess th contribution of 2-DG-stimulated gastric acid secretion in the 2-DG-induced SLI rise 2-DG was infused during the infusion of the H2-receptor antagonist cimetidine (3.0 mg/kg . h). Plasma SLI, nevertheless, increased significantly from a mean baseline of 112 +/- 6 pg/ml to a mean peak of 158 +/- 19 pg/ml (P less than 0.005) at 20 min, although the magnitude of the response was substantially reduced (P = NS). These observations suggest that in the conscious dog, 2-DG stimulates SLI secretion in part via cholinergic mechanism.
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PMID:Effect of 2-deoxy-D-glucose on plasma somatostatin levels in conscious dogs. 611 May 37

Seven double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated and denervated mucosa at the same time in the same animal. Stimulation was done by food, a mixture of liver, heart and bonemeal, 10 g/kg. Cimetidine, 25, 50, 100, 200, and 400 mg; atropine, 0.031, 0.125, 0.5 and 1.0 mg; somatostatin, 0.5, 1.0, and 2.0 micrograms/kg/h; and secretin 2 U/kg/h, were given 60 min after the meal, one single dose on each day. Atropine and somatostatin lowered pepsin secretion in both pouches, significantly more in denervated mucosa for all doses of somatostatin and for the lower doses of atropine. Higher doses of atropine nearly abolished the secretion in both pouches. Cimetidine lowered pepsin output only in denervated mucosa. In innervated mucosa the output was unchanged or significantly increased (50 mg) by cimetidine. Secretin increased pepsin output significantly in both pouches, more in innervated mucosa. When the infusion of somatostatin was topped, a marked rebound effect was seen in the innervated pouch.
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PMID:The influence of hormones and drugs on gastric pepsin secretion. The role of vagal innervation. 611 89

The effects of various pharmacological agents on bile acid-induced fluid secretion, mucus secretion, and mucosal injury were investigated using a perfusion technique in rabbit colon. Atropine markedly reduced and carbachol potentiated the fluid secretion, mucus output, and mucosal damage observed during bile acid perfusion. In contrast, pretreatment of the colonic mucosa with lignocaine and parenteral administration of methysergide and somatostatin produced a modest reduction in the fluid secretory response without apparent effects on mucus output or mucosal damage. These results suggested that cholinergic agonists and antagonists influence the mucosal resistance to bile acid-induced injury possibly through their effects on mucus secretion. Increasing or decreasing mucosal resistance to the detergent effects of bile acids appeared to have marked effects on the magnitude of induced fluid secretion. A minor reduction in overall secretory response to bile acids was also apparent with agents not influencing mucus secretion or mucosal injury.
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PMID:Pharmacological inhibition of chenodeoxycholate-induced fluid and mucus secretion and mucosal injury in the rabbit colon. 612 21

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49 +/- 10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49 +/- 10 to 23 +/- 9 pM, whereas gastrin and insulin levels rose from 9 +/- 2 and 140 +/- 14 pM to 48 +/- 11 and 370 +/- 91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin level rose again and peaked at around 60 min after feeding (110 +/- 24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCl secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.
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PMID:Plasma levels of somatostatin following a test meal in dogs. Initial atropine resistant vagally mediated decrease of somatostatin levels and increase of gastrin and insulin levels. 612 67

The regulation of gastrin and somatostatin secretion by intramural neurons was examined in the isolated vascularly perfused rat stomach. The optimal modalities of transmural electrical stimulation of the antrum were established to be 40 V and 10 Hz. Stimulation at increasing cycle durations (0.1-4 ms) caused increasing gastrin secretion that was progressively more resistant to atropine. The maximal gastrin response to 4-ms cycles was equal to the maximal response to methacholine. However, the response to methacholine was inhibited 70-90% by atropine, whereas the response to 4-ms cycles was inhibited by 15% only. Stimulation at all cycle durations caused a decrease in somatostatin secretion. Atropine converted the decrease to an increase, from which it was concluded that before atropine somatostatin secretion was the net result of cholinergic inhibition and noncholinergic stimulation of somatostatin. The results indicate that cholinergic and noncholinergic intramural neurons are predominantly but not exclusively activated by 0.1- and 4-ms cycles, respectively. The existence of distinct neurons was supported by results of stimulation of preganglionic vagal fibers with 0.2- and 4-ms cycles. The findings are consistent with a model according to which gastrin secretion is regulated by two interdependent intramural neurons: a cholinergic neuron that stimulates gastrin secretion indirectly by inhibition of somatostatin secretion and a noncholinergic neuron that stimulates gastrin secretion directly by release of a peptide stimulant, probably bombesin.
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PMID:Regulation of gastrin and somatostatin secretion by cholinergic and noncholinergic intramural neurons. 612 24

Regulation of somatostatin (SS) secretion was studied in an in vitro system using collagenase-dispersed cells from fetal rat hypothalamus maintained in long term monolayer culture. Cultured cells exhibit a measurable basal secretion of immunoactive SS (SSLI) which can be augmented by carbachol, acetylcholine, or oxotremorine. The EC50 for carbachol is about 1 microM. Atropine, but not hexamethonium, antagonizes the action of cholinergic agonists. Cobalt or tetrodotoxin pretreatment diminishes basal secretion and eliminates the response to carbachol. Serotonin, several serotonin agonists, and gamma-aminobutyric acid (GABA) suppress carbachol-induced secretion. The GABA blockers bicuculline or picrotoxinin reverse the effect of added GABA and by themselves also augment SSLI secretion. Picrotin is inactive. The direct response to either bicuiculline or picrotoxinin is prevented by cobalt or tetrodotoxin treatment. These observations are consistent with the presence of a muscarinic cholinergic receptor which acts by a mechanism depending on an action potential and calcium influx to enhance the release of SSLI from neurosecretory cells. The data also support the conclusion that GABAergic transmission occurs within the cultures to tonically inhibit SSLI secretion. GABAergic, cholinergic, and serotoninergic systems may thus interact at the level of the hypothalamus to modulate SS secretion in vivo and thereby influence anterior pituitary release of GH and TSH.
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PMID:Muscarinic cholinergic stimulation of somatostatin secretion from long term dispersed cell cultures of fetal rat hypothalamus: inhibition by gamma-aminobutyric acid and serotonin. 612 32

The effect of somatostatin on lateral hypothalamic self-stimulation was investigated in atropine- and methysergide-pretreated rats. Somatostatin markedly decreased the self-stimulation rate of the animals. Atropine in a dose which had no action on self-stimulation partly antagonized the effect of somatostatin. Methysergide potentiated the somatostatin-induced depression of self-stimulation behavior. These results suggest that the central cholinergic and serotoninergic systems may play a role in the somatostatin-induced inhibition of self-stimulation.
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PMID:The effect of somatostatin on self-stimulation behavior in atropine- and methysergide-pretreated rats. 613 93

Bombesin, acetylcholine, prostaglandins and somatostatin are all thought to be involved in the regulation of gastrin release and gastric secretion. We have studied the effects of low doses of atropine, 16-16(Me)2-prostaglandin E2 (PGE2) and somatostatin-14 on bombesin-stimulated gastrin release and gastric acid and pepsin secretion in conscious fistula dogs. For reference, synthetic gastrin G-17 was studied with and without somatostatin. Bombesin, in a dose-related manner, increased serum gastrin, which in turn stimulated gastric acid and pepsin secretion in a serum gastrin, concentration-dependent manner. Somatostatin inhibited gastrin release by bombesin as well as the secretory stimulation by G-17; the combination of sequential effects resulted in a marked inhibition of bombesin-stimulated gastric acid and pepsin secretion. PGE2 also strongly inhibited gastrin release and acid and pepsin secretion. Atropine had no significant effect on gastrin release, but greatly inhibited gastric secretion. Thus somatostatin and PGE2 inhibited at two sites, gastrin release and gastrin effects, while atropine affected only the latter.
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PMID:Somatostatin, prostaglandin E2 and atropine inhibition of the gastric actions of bombesin in the dog. 614 3


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