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)

Intrarenal infusion of somatostatin in anesthetized dogs produced a prompt increase in urine flow in association with a decrease in urinary osmolality and an increase in free water clearance. These changes occurred in the absence of changes in arterial pressure, renal plasma flow, osmolar clearance, electrolyte excretion or cyclic AMP excretion. The diuretic effect occurred primarily in the infused kidney indicating a direct intrarenal action rather than suppression of vasopressin secretion. This diuretic action of somatostatin may result from inhibition of the action of vasopressin on the renal medulla but other possible mechanisms cannot be excluded.
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PMID:An intrarenal effect of somatostatin on water excretion. 4 71

The ability of somatostatin to modify the water premeability of the toad bladder was examined. Somatostatin had a small effect on basal water flow and antagonized the hydrosmotic effect of vasopressin. Water flow induced by cyclic AMP was enhanced. These results may explain the diuretic and hyposthenuric effects of somatostatin in vivo.
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PMID:Antagonism of vasopressin-induced water flow by somatostatin. 10 4

Cyclic somatostatin was administered intravenously on eight occasions to five consecutive patients with massive haemalemesis due to oesophageal varices. The doses administered with 0--250 micrograms as bolus, followed by 100--250 micrograms per hr during 2--12 hrs. The source of bleeding was determined by endoscopy. The volume of bleeding was estimated from the clinical condition of the patient and by gastric irrigation and iced water. The bleeding stopped immediately on all occasions when somatostatin was administered. It is suggested that the effect is due to the ability of somatostatin to reduce regional splanchnic blood flows and portal pressure.
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PMID:Treatment of bleeding oesophageal varices with somatostatin. 31 31

The chemistry, localisation, release and effects of gastrointestinal hormones and some related peptides are surveyed. Their main presumed physiologic actions are: gastric acid and pepsin secretion are stimulated by gastrin and to a less degree by secretin. Acid secretion is inhibited by bulbo-enterogastrone and GIP. Biliary water and electrolytes are augmented by gastrin, CCK-PZ, secretin and VIP and inhibited by Substance P. Pancreatic bicarbonate and enzyme secretions are stimulated by secretin and CCK-PZ, especially in combination. Lower oesophageal and antral motility and tonus are elevated following gastrin and motilin; the gallbladder and small intestine empty following CCK. Gastrin regulates gastrointestinal, and CCK pancreatic, tissue growth. Somatostatin inhibits all gut hormones. All peptides are vasoactive within the splanchnic area, each one in a specific manner.
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PMID:Gastrointestinal hormones. 35 98

Since both TRH and somatostatin (SRIF) are localized to the ventromedial hypothalamic nucleus, a region known to be involved in control of food intake, the possibility that these peptides might alter food intake was evaluated. The peptides were dissolved in 0.9% NaCl and injected into the 3d ventricle in a volume of 2 micron1 in animals bearing 3d ventricular cannulae. Food and water had been removed from the cages the night before and the intake was measured at 1 and 6 h after injection. Control injections of 0.15M NaCl or glutathione (3 nmoles) had no effect on food or water intake. At a dose of 3 nmoles, LHRH, SRIF, and TRH suppressed water intake alh. Lowering the dose of LHRH and SRIF to 0.6 nmoles led to loss of this inhibition but the suppressive effect of TRH, which was more pronounced at the higher dose than that of the other two peptides, persisted. Lowering the dose of TRH to 0.3 nmoles led to loss of the inhibitory effect. The dose of 3 nmoles of LHRH did not suppress food intake but this dose of both SRIF and TRH had a significant suppressive effect on food intake at 1 h. There was no suppressive action of a lower dose of 0.6 nmoles of SRIF, but TRH was still effective to suppress food intake at this dose. A dose of 0.3 nmoles of TRH had no effect on food intake. It is suggested that TRH, and possibly SRIF may play a physiological role in control of food intake, perhaps by altering the neural activity within the ventromedial nucleus.
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PMID:Suppression of feeding and drinking activity in rats following intraventricular injection of thyrotropin releasing hormone (TRH). 40 33

Twenty-five years ago we described an extraction procedure for porcine secretin in which the intestinal tissue is briefly boiled in water and then extracted with dilute acid at low temperature. Boiling in water, which inactivates proteolytic enzymes, does not extract secretin, and extraction with acid in the cold will minimize cleavage of acid labile peptide structures. This extraction procedure has formed the basis for the isolation not only of secretin but also of cholecystokinin-pancreozymin (CCK) and, in collaboration with other laboratories, of the vasoactive intestinal peptide (VIP), the gastric inhibitory peptide (GIP), and motilin. Recently it has been used for the isolation of an N-terminally extended somatostatin from intestinal tissue, and of a peptide, from both nonantral gastric and intestinal tissues, with gastrin-releasing and probably cholecystokinin-releasing properties. A technique has been worked out permitting the chemical analysis, in certain cases, of polypeptide hormones in the presence of other polypeptides, the polypeptide mixture being exposed to fragmentation conditions known to result in characteristic hormone fragments, which are then extracted and quantitated. The technique can also be useful for the isolation of previously unknown peptides by identifying fragments of such and tracing them back to their peptides of origin.
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PMID:Some contributions to the chemistry of the gastrointestinal hormones. 45 17

Six conscious intact dogs were studied to evaluate the interactions of somatostatin (SRIF) with exogenous antidiuretic hormone arginine vasopressin (AVP). SRIF administration caused a significant increase in free water clearance compared to a vehicle-treated group: -0.91 (+/- 0.41 SD) ml/min to 0.21 (+/- 0.32 SD) ml/min in the experimental group (P less than 0.01) versus 0.21 (+/- 0.81 SD) ml/min to -0.21 (+/- 0.68 SD) ml/min in the control (P greater than 0.5). Six conscious, thyroparathyroidectomized dogs were studied to test the interaction of SRIF and parathyroid extract (PTE). There were no significant changes in the phosphaturic and hypocalciuric effects of PTE with SRIF administration. We conclude that acute systemic SRIF administration interferes with the antidiuretic action of AVP, probably at the renal-tubular level, but does not antagonize the renal actions of PTE.
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PMID:Interaction of somatostatin with PTH and AVP: renal effects. 49 45

The role of nerves that liberate vasoactive intestinal polypeptide (VIP) in the porcine pancrease as mediators of the atropine-resistant action of the vagus on flow and bicarbonate (HCO3) secretion was examined. Efferent electrical stimulation of the vagus in atropinized pigs produced a profuse flow of pancreatic juice with high HCO3 content concomitantly with a significant increase in pancreatic VIP output from 13 to 113 fmol/min. Intravenous administration of somatostatin (SRIF) during continuous electrical vagal stimulation caused a parallel suppression of the VIP release and the pancreatic fluid and HCO3 secretion to prestimulatory values. The SRIF-induced reduction in fluid and HCO3 secretion seemed to be mediated via an inhibition of the VIP release rather than through a direct effect on the exocrine cells, inasmuch as SRIF did not influence the VIP-provoked exocrine response from the in vitro isolated perfused porcine pancreas. The results support the view that VIP is transmitter in the vagally induced atropine-resistant water and HCO3 secretion from the porcine pancreas.
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PMID:Vasoactive intestinal polypeptide in vagally mediated pancreatic secretion of fluid and HCO3. 51 50

Nalpha-Tyrosyl-somatostatin was synthesized and proved to be homogeneous. Radioiodination of this tyrosine-containing somatostatin analogue by either the lactoperoxidase method or the chloramine T method led to the formation of crude iodinated compound, which was purified by ion exchange chromatography on CM-Sephadex C-25 using a linear ammonium acetate buffer gradient. This purification process was found to be satisfactorily reproducible and suitable for the preparation of 125I-Nalpha-tyrosyl-somatostatin. Using the purified 125I-somatostatin analogue, radioimmunoassay for somatostatin was performed and the assay system was proved to be sensitive and specific for somatostatin. Immunoassays of hot-water extracts of porcine and tupaia brain, pancreas, stomach and various regions of the intestine in the system revealed that those tissues contained immunoreactive somatostatin at various concentrations. Of the results, it was remarkable that somatostatin immunoreactivity was found in the ileum, middle colon and rectum in both animals, although the concentration were lower when compared with those in the stomach, duodenum and jejunum.
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PMID:Somatostatin radioimmunoassay with 125I-Nalpha-tyrosyl-somatostatin. 63 59

The effects of somatostatin on the secretions of the exocrine pancreas were studied in anesthetized and conscious fistula rats. Somatostatin resulted in a dose-dependent decrease of basal secretion (flow, bicarbonate, protein) in conscious rats. In anesthetized rats, basal secretion was initially augmented by bolus injections of 10 to 50 microgram per kg and was subsequently decreased by venous infusions of somatostatin at 1.5 to 100 microgram.kg-1.hr-1. This inhibition, which was poorly dose dependent, was greater for protein secretion than for that of water and electrolytes. Somatostatin inhibited caerulein-stimulated protein secretion by 40 to 50% but had no effect on secretion stimulated by exogenous and endogenous secretin. Somatostatin markedly inhibited secretion stimulated by 2-deoxyglucose and by electrical stimulation of the vagus nerves in a dose-dependent fashion (protein and bicarbonate exhibited a maximal inhibition of 85%). Acetylcholine-stimulated secretion was also inhibited by somatostatin, but the maximal inhibitions observed were only 505 for protein and 60% for bicarbonate. These findings agree with the hypothesis that somatostatin infusion leads to both a decrease of acetylcholine release at nerve endings and to a direct inhibition at the level of pancreatic effector cells.
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PMID:Effects of somatostatin on the external secretion of the pancreas of the rat. 70 Mar 25


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