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)

Anterior pituitary glands from broiler fowl were incubated alone or with hypothalamic tissue in medium containing either serotonin or serotoninergic drugs, acetylcholine or cholinergic drugs, and the release of prolactin (Prl) and growth hormone (GH) measured by homologous radioimmunoassays. The neurotransmitters and drugs affected the release of hormones from the pituitary gland only when hypothalamic tissue was also present. Serotonin and its agonist quipazine stimulated the release of Prl and inhibited release of GH in a concentration-related manner. The antagonist methysergide blocked the effects of serotonin and quipazine on Prl. Acetylcholine and its agonist pilocarpine also stimulated release of Prl and inhibited release of GH in a concentration-related manner. Atropine blocked these responses. The results show that serotonin and acetylcholine affect pituitary hormone secretion by acting on the hypothalamus. They may stimulate the secretion of a Prl releasing hormone and somatostatin.
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PMID:Serotonin and acetylcholine affect the release of prolactin and growth hormone from pituitary glands of domestic fowl in vitro in the presence of hypothalamic tissue. 614 26

Somatostatin has previously been shown to reduce nutrient absorption from the human jejunum. These studies were designed to examine whether changes in intestinal motility may be responsible for the inhibitory effect of somatostatin on intestinal absorption. Using triple-lumen perfusion techniques in healthy volunteers, somatostatin infusion (8 micrograms/kg/h) prolonged mean transit time from 9 to 16 min in a 30-cm jejunal test segment as estimated from dye dilution curves. Somatostatin infusion significantly reduced jejunal fructose absorption. Atropine (10 micrograms/kg/h, i.v.) caused a similar prolongation of mean transit time in the perfused jejunum. However, unlike somatostatin, atropine significantly increased fructose absorption. The observation that somatostatin and atropine affect absorption in opposite ways while prolonging intestinal transit time in a similar fashion suggests that the effects of somatostatin and atropine are due to a direct influence on absorption at the mucosal level that is independent of any effect on intestinal motility.
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PMID:Effect of somatostatin and atropine infusion on intestinal transit time and fructose absorption in the perfused human jejunum. 614 9

The effects of pretreatment with atropine, haloperidol and phenoxybenzamine on somatostatin-induced antiamnesia were investigated. Somatostatin itself blocked electroconvulsive shock (ECS)-induced amnesia. The receptor blockers per se had no influence on the ECS-induced avoidance latency. Atropine and haloperidol did not inhibit somatostatin-induced antiamnesia, whereas phenoxybenzamine blocked it completely. The results suggest that the central noradrenergic system plays an important role in the mediation of the antiamnesic action of somatostatin.
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PMID:Phenoxybenzamine antagonizes somatostatin-induced antiamnesia in rats. 614 3

In the present study the release of somatostatin-like immunoreactivity (SLI) was evaluated in vitro from isolated rat antral and fundic mucosa and from biopsy specimens of human antral mucosa. Perifusion of antral mucosa with Earle's balanced salt solution showed a pH-dependent release of SLI. SLI release did not change in response to a reduction from pH 7 during the baseline period to pH 3, whereas a significant increase occurred when the pH was changed to 2.5 or 2, respectively. Fundic SLI release remained at baseline levels during the decrease of the pH value of the buffer solutions. Atropine at doses of 10(-6) to 10(-4) M did not alter acid-induced SLI release from the isolated antral mucosa, suggesting different mechanisms in vitro compared to the acid-induced SLI release in vivo. SLI release from human mucosa was 450 +/- 217 pg/min X mg wet weight in response to perifusion with the buffer pH 2 in 7 control subjects. No significant difference was observed in patients with duodenal ulcer or acute gastritis, whereas gastric ulcer patients had significantly lower values (66 +/- 44) compared to controls and duodenal ulcer patients. These data do not support the hypothesis that impaired somatostatin production and release might be a pathogenetic factor for gastric acid hypersecretion and development of duodenal ulcer.
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PMID:Somatostatin release from perifused rat and human gastric mucosa. 614 69

1. The effects of some putative non-adrenergic, non-cholinergic transmitters have been studied on longitudinal and circular smooth muscle from the stomach of the rainbow trout, Salmo gairdneri. 2. ATP, adenosine and vasoactive intestinal polypeptide (VIP) on certain occasions inhibited the activity of the stomach smooth muscle; ATP and adenosine only circular muscle. VIP both longitudinal and circular muscle. 3. Neurotensin produced a contraction, which in strips from the cardiac stomach in most cases occurred after the exposure to the peptide; this might be a rebound contraction after an inhibition which could not be recorded with the experimental set-up. 4. Bombesin, 5-hydroxytryptamine and substance P produced dose-dependent contractions over a wide dose range. Somatostatin and enkephalin contracted the preparations only in the highest doses tested (10(-9) moles, 10(-8) moles). 5. Atropine did not reduce or abolish the response to any of the substances tested, indicating that their effects are not via cholinergic neurons, which innervate the smooth muscle. 6. Of the substances tested ATP, adenosine, VIP and neurotensin may be involved in the inhibitory vagal non-adrenergic, non-cholinergic innervation of the rainbow trout stomach.
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PMID:The effects of putative non-adrenergic, non-cholinergic autonomic transmitters on isolated strips from the stomach of the rainbow trout. Salmo gairdneri. 618 77

We used acute anesthetized dogs to investigate the role of cholinergic receptors in the relationship between antral immunoreactive (I) gastrin release and antral motility. Electrical stimulation of extrinsic nerves via the cervical vagus or the nerve of Latarjet appeared to increase I gastrin release and antral motility by separate pathways as blockade of muscarinic receptors, i.e., atropinization inhibited motility but did not alter I gastrin release. On the other hand, blockade of nicotinic receptors by hexamethonium treatment obliterated I gastrin release induced by stimulation of the extrinsic nerves but only reduced motility. Field stimulation of intrinsic nerves via serosal electrodes also increased both I gastrin release and local motility. Since hexamethonium treatment only slightly reduced both I gastrin release and motility and atropinization eliminated both during field stimulation, the presence of a muscarinic receptor in the final pathway for each is proposed. Atropine eliminated carbachol-induced I gastrin release and motility increases, even in the presence of nerve blockade by tetrodotoxin. This suggests that this muscarinic receptor is on the smooth muscle cell itself and possibly on the gastrin cell. However a proposed role of the somatostatin cell in controlling gastrin release is also consistent with these data. Thus, both an intrinsic cholinergic and a separate extrinsic noncholinergic pathway are involved in antral release of I gastrin but initiation of motility appears to involve a final common pathway terminating in a muscarinic receptor on the smooth muscle cell.
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PMID:Cholinergic control of canine antral immunoreactive gastrin release and motility. 712 12

1. The efficacies of some standard preparations of CCK were compared and the effects of some drugs and peptide hormones on the responsiveness of the rabbit isolated gall-bladder to cholecystokinin were studied with an established automatic method of estimating cholecystokinin. 2. Atropine, propranolol, phentolamine mesylate and lignocaine were shown to have no effect on the responsiveness of the rabbit isolated gall-bladder. 3. Glucagon, somatostatin, pentagastrin, pancreatic polypeptide, motilin and the Karolinska preparation of secretin had no effect on the preparation alone and caused only slight changes when given with cholecystokinin. 4. The Boots preparation of secretin exhibited a small cholecystokinin effect when given alone, but considerably inhibited cholecystokinin-induced contractions. 5. The desulphated C-terminal octapeptide of cholecystokinin also exhibited inhibitory effects.
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PMID:Effects of some drugs and peptide hormones on the responsiveness of the rabbit isolated gall-bladder to cholecystokinin. 715 34

The effects of electrical stimulation of the vagus at varying pulse widths on the release of immunoreactive VIP (IR-VIP) and IR-gastrin have been investigated, using the isolated perfused rat stomach preparation. Electrical stimulation of vagal trunks at a pulse width of 0.1 msec duration yielded no change in basal IR-VIP levels whereas a pulse width of 5.0 msec produced a prompt sustained increase. Stimulation at either pulse width evoked gastrin release. Atropine blocked the vagal release of IR-gastrin but not IR-VIP whereas hexamethonium blocked both responses. Exogenously administered porcine VIP, at concentrations mimicking endogenously released levels, was used in an attempt to reproduce the effects observed by vagal stimulation. Exogenous VIP had no effect on gastrin or somatostatin-like immunoreactivity (SLI) release. These in vitro studies support a role for VIP as a neurotransmitter released from the stomach by low-threshold non-cholinergic vagal fibres, but involving autonomic ganglia.
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PMID:Vagal release of IR-VIP and IR-gastrin from the isolated perfused rat stomach. 727 50

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

We studied the release of immunoreactive somatostatin, VIP, and galanin during net aboral propulsive complexes (NAP) in isolated, perfused, 80-cm segments of porcine ileum. Net aboral propulsive complexes were induced by controlled infusion of liquid (perfusion medium, 3.5 ml/min) into the proximal opening of the ileum segment. In response to liquid infusion, the ileum segments generated propulsive complexes rapidly propagating along the entire segment in the aboral direction, resulting in emptying of the luminal contents. The NAPs occurred with an average interval of 7 minutes. The concentrations of galanin, somatostatin, and VIP in the venous effluent, which in control experiments without luminal infusion did not change, increased significantly (by 63.6 +/- 23.7%, 43.8 +/- 31.8%, and 38.8 +/- 14.6%, respectively) during NAPs and emptying. Atropine (10(-6) mol/l) and hexamethonium (10(-5) mol/l) abolished both NAP generation and peptide responses. It is concluded that the enteric neuropeptides, somatostatin, VIP, and galanin, all of which have pronounced intestinal motor effects, may participate in the generation of net aboral propulsive complexes in the ileum of the pig, possibly mainly in descending relaxation.
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PMID:Release of immunoreactive somatostatin, vasoactive intestinal polypeptide (VIP), and galanin during propulsive complexes in isolated pig ileum. 768 99


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