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)

Immunoreactive GH release-inhibiting factor [somatostatin (SRIF)] was detected in hypothalamus, extrahypothalamic brain, pancreas, and stomach extracts of the rat, pigeon, tortoise, frog, teleost (cichlid), and elasmobranch (dogfish) and in the whole brain of the cyclostome (hagfish). The SRIF concentration was higher in the pancreas and gastrointestinal tract than in the hypothalamus and extrahypothalamic brain in most species. Extracts of the various tissues from the different species assayed in serial dilutions gave displacement curves parallel to those of synthetic mammalian SRIF. Cation exchange chromatography of hypothalamic extracts from the various species revealed two major immunoreactive peaks, one of which correpsonds to synthetic SRIF in elution volume, the other being less basic. Affinity chromatography-purified immunoreactive SRIF from frog brain, pancreas, and stomach extracts coeluted with synthetic SRIF in high pressure liquid chromatography. The results indicate that immunoreactive SRIF in various tissues and in different vertebrates is indistinguishable and suggest that there has been no change in the molecule during at least 400 million yr of evolution.
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PMID:Phylogenetic and anatomical distribution of somatostatin in vertebrates. 49 75

The effect of vasoactive intestinal peptide (VIP) was studied on the release of somatostatin (SRIF) from slices of several regions of the rat brain in vitro. VIP induced a dose-dependent inhibition of SRIF release from mediobasal hypothalamic slices but did not interfere with SRIF release from preoptic area, amygdala or cortex. VIP inhibition had an apparent affinity: Kd = 6.8 +/- 3.9 x 10(-11) M. Secretin had a similar effect but at 600-fold higher concentrations (Kd secretin = 4.2 +/- 0.6 x 10(-8) M). Gucagon was ineffective in concentrations ranging from 10(-10) M to 10(-7) M. The data are consistent with a role of VIP in the hypothalamic control of growth hormone secretion.
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PMID:Vasoactive intestinal peptide inhibits release of somatostatin from hypothalamus in vitro. 51 Mar 82

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

In 9 fetuses, 9 to 24 weeks-old, the occurrence and relative distribution of argentaffin cells, as well as of cells immunoreactive to somatostatin (SRIF), glucagon-like polypeptide (GLI), pancreatic polypeptide (PP) and substance P (SP) were studied in five segments of the colon (appendix, cecum, ascending colon, descending colon, and rectosigmoid). For each colonic segment, data concerned with the occurrence of endocrine cells were expressed either as mean absolute numbers of specific cells per entire mucosal section, or as cell densities per mm3 of mucosa after calculation of the mucosal volume of the sections. Argentaffin, GLI, SRIF and PP immunoreactive cells are all present in relatively large numbers, scattered along the entire length of the colonic mucosa as early as the 9th-10th week of gestation, whereas substance P-containing cells occur sporadically and first appear during the 4th-17th week. Until the 20th week, with progressing embryonic development, an increase was determined in absolute numbers per section of all types of endocrine cells in all segments of the colon. This observation is clearly related to the general growth of the colonic mucosa, since cell densities per mm3 of mucosa do not greatly change or even decrease during gestation. However, it is possible that densities of argentaffin, GLI and BPP cells increase in the appendix around the 14th-17th week of gestation. Between 20th and 24th weeks, absolute numbers of cells per section remain stable or slightly increase, while cell densities tend rather to decrease in all segments. These data demonstrate that some endocrine cells are present very early in the human fetal colon, but their functional significance remains to be elucidated.
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PMID:Ontogeny and distribution of certain oendocrine cells in the human fetal large intestine. Histochemical and immunocytochemical studies. 51 32

Hypothalamic somatostatin release was investigated in the rat to elucidate the mechanism of anesthetic action on growth hormone (GH) release from the pituitary. Intraperitoneal injection of sodium pentobarbital (5 mg/100 gm B.W.) significantly elevated serum GH levels and increased hypothalamic somatostatin concentration from basal values of 0.98 +/- 0.01 to 1.21 +/- 0.06 ng/mg wet wt. In contrast, urethane (150 mg/100 gm B.W., IP) administration lowered serum GH levels and hypothalamic somatostatin concentration (0.64 +/- 0.04 ng/mg wet wt.). However, the mean concentration of pancreatic somatostatin showed no change in either case. In rats receiving passive immunization with 0.5 ml rabbit antiserum to somatostatin (SRIF-AS), serum GH levels were significantly increased (67.5 +/- 12.3 ng/ml) and did not differ from those in the group treated with normal rabbit serum (NRS) plus pentobarbital (101.3 +/- 18.5 ng/ml). However, serum GH levels in rats injected with SRIF-AS plus pentobarbital were increased to higher values than in rats given SRIF-AS alone. When urethane was administered to rats after passive immunization with SRIF-AS, urethane-induced suppression of serum GH levels was markedly inhibited (5.5 +/- 2.0 vs. 33.5 +/- 7.5 ng/ml). These results suggest a possibility that the changes in serum GH levels observed with pentobarbital or urethane administration may be induced at least in one part by somatostatin released from the hypothalamus.
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PMID:Effect of pentobarbital and urethane on the release of hypothalamic somatostatin and pituitary growth hormone. 52 Oct 10

The administration of small doses of somatostatin (SRIF) (0.01 and 0.1 microgram) into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS). In contrast, the higher doses of SRIF (1.0 and 10.0 microgram) caused movements to be uncoordinated and frequently induced more severe difficulties in motor control such as contralateral hemiplegia-in-extension which restricted or completely prevented the expression of normal behavioral patterns. As a result, the animals appeared drowsy and inhibited. Analysis of the sleep-waking cycle revealed prolonged periods of a shallow SWS while REM sleep and deep SWS were markedly reduced; electroencephalogram recordings revealed periods of dissociation from behavior. The administration of endocrinologically inactive as well as the active analogues of SRIF failed to induce effects comparable with those observed after the administration of the same dose of the native hormone (10.0 microgram).
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PMID:Neostriatal administration of somatostatin:differential effect of small and large doses on behavior and motor control. 55 30

In rats the influence of arresting free motions (= controls; mild stress) and of restraint (= severe stress) without and with additional somatostatin (SRIF) on gastric secretion, mucosal microcirculation and stress ulcer formation was studied. Severe stress alone reduces volume, acid and pepsin secretion, acid concentration, aminopyrine clearance and ratio. The ulcer index is elevated. Under both conditions SRIF inhibits in a dose-dependent manner volume and acid secretion, and ulcer incidence is lower. The interaction between severe stress and the antiulcer component of SRIF is characterized as non-competitive. Under these conditions and a continuous infusion of SRIF (10.0 microgram/kg.h over 8 h) acid concentration, acid and pepsin secretion fall subtotally, ulcer index to 50 percent of vehicle (saline) treated rats, if gastric fistula drains juice outside stomach. Microcirculation and serum gastrin are unchanged. In animals with closed fistula ulcer index is reduced by 85 percent, average gastrin again is unchanged. It is concluded that stress ulcers develop at a low secretory and microcirculatory state of gastric mucosa. The prophylactic effect of SRIF results from direct inhibition of parietal and chief cells and additional yet unknown factors.
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PMID:Anti-stress ulcer and anti-secretory effect of somatostatin in rats -- failure to suppress serum gastrin. 56 56

Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.
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PMID:Somatostatin therapy of acute experimental pancreatitis. 60 91

Total immunoreactive glucagon (IRG) and immunoreactive glucagon of A cell origin (IRGa) were measured in the serum of normal, sham-operated and depancreatized rats, after the administration of three glucagon antagonists: insulin (5--200 mU/rat/h), somatostatin (SRIF; 100 microgram/kg/h) and antiglucagon serum (AGS, enough to bind three times the calculated total amount of circulating IRG). Since no differences were noted between the responses of normal and sham-operated animals, the values were pooled and used as controls. Pancreatectomy caused a significant increase in serum glucose, IRGa and total IRG and a significant decrease in serum insulin. AGS and SRIF significantly decreased serum glucose in control, but not in depancreatized rats, even though SRIF caused a significant decrease of IRGa in all animals. SRIF significantly decreased plasma insulin in control rats, but did not modify total IRG secretion in either groups. In control rats the minimum effective hypoglycaemic dose of insulin (5 mU/rat/h) may have decreased serum IRGa, but not total IRG. At higher doses (20 mU/rat/h) insulin stimulated glucagon secretion. In depancreatized animals, higher doses of insulin (200 mU/rat/h) were needed to lower serum glucose. On the other hand, a dose of 100 muU/rat/h was sufficient to lower the serum IRG. We conclude that although hyperglucagonaemia may contribute to the hyperglycaemia of the untreated depancreatized rats, the excessive secretion of glucagon is secondary to insulin insufficiency and that, at least in this animal model, the hypoglycaemic action of insulin is only minimally dependent upon its ability to suppress glucagon secretion.
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PMID:The serum glucose response to glucagon suppression with somatostatin, insulin or antiglucagon serum in depancreatized rats. 62 33

The latency to tail-flick response in the rat was significantly prolonged by cerebroventricular infusion of 1.0 microgram of somatostatin (SRIF) and more so with 10.0 microgram. The D-tryptophan analog was less effective than native SRIF. Pretreatment with naloxone eliminated analgesia but not seizures induced by SRIF. Recording of the EEG activity enabled determination of the specific state of the sleep-waking cycle in which the repeated tail-flick responses were tested: latency was generally longer in both control and test animals when tail immersion was performed during the state of sleep or drowsiness rather than during the awake state. Although animals receiving SRIF were less likely to fall asleep between subsequent test trails, the average latency was actually longer than after control saline infusion when the animals slept more. SRIF, unlike other releasing factors and peptides tested, showed significant activity in an opiate radioreceptor assay. The blockade of SRIF action by naloxone pretreatment, along with binding of SRIF to opiate receptors in vitro, suggest opiate receptors to be involved in the mediation of analgesia observed in present study.
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PMID:Opiate-like naloxone-reversible actions of somatostatin given intracerebrally. 63 75


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