Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of growth hormone-releasing factor (GHRF) on growth hormone (GH) secretion were studied in beef calves after hypophysial stalk transection (HST). Peripheral GH concentration during surgery was elevated for 60 min after the initiation of anesthesia to 15 ng/ml, which was greater than plasma levels after HST and during the recovery period (0-30 hr mean, 3 ng/ml; P less than 0.05). Episodic GH secretion normally seen in sham-operated controls (SOC) was abolished after HST. Before HST, calves responded to 80% of the GHRF challenges, whereas after HST calves responded to every challenge of GHRF with an increase in plasma GH. A dose of 0.067 microgram human pancreatic (hp) hpGHRF(1-40)OH/kg body wt 3 days after HST increased plasma GH to 55 ng/ml from a control period mean of 5 ng/ml (P less than 0.04). On Day 8, HST calves received two injections of 0.067 microgram hpGHRF/kg body wt at 3-hr intervals, with feeding 70 min after the first injection. During two preinjection control periods, basal GH averaged less than 4 ng/ml and increased to 17 (P less than 0.02) and 9 (P less than 0.04) ng/ml immediately after the first and second injection of hpGHRF, but the response declined over the 8-day period after surgery. On Days 19 and 20, the HST calves were infused iv with 0.033 and 0.067 microgram somatostatin(SS)-14 (SRIH)/kg body wt, during which a pulse injection of 0.067 microgram hpGHRF/kg body wt was administered. GH increased to 9 and 5 ng/ml during the 0.033- and 0.067-microgram SRIH infusions after GHRF; no somatotropic rebound was observed after the SRIH was discontinued as was seen in the animals while the hypothalamic-hypophysial connections were intact. Five and six months after HST the responses to two analogs of rat hypothalamic GHRF were similar to those in SOC calves. These results indicate that HST calves responded to exogenous GHRF with an abrupt increase in plasma GH, but GH response to GHRF during SRIH infusion was greatly inhibited.
 ...
PMID:Effects of growth hormone-releasing factor and somatostatin on growth hormone secretion in hypophysial stalk-transected beef calves. 290 52

Neurotensin (NT) differentially altered ethanol-induced anesthesia as measured by duration of loss of righting response or by blood ethanol levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to ethanol. At doses of 5-500 ng i.c.v., NT increased ethanol sensitivity in SS mice, but not in LS mice, as measured by blood ethanol concentrations at loss of righting response. At higher doses, 0.5-10 micrograms i.c.v., NT enhanced the sensitivity of both SS and LS mice to ethanol-induced anesthesia. The hypothermic effect of ethanol determined at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced ethanol-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for ethanol in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogues, N-acetyl-NT8-13, and [D-Trp11]-NT but not NT1-8 enhanced the anesthetic action of ethanol in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin and corticotropin releasing hormone (CRF) were not effective in enhancing ethanol-induced anesthesia in LS or SS mice. CRF appeared to decrease ethanol sensitivity in LS but not in SS mice. Beta-Endorphin (beta-END) markedly increased the ethanol sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g. 0.5-1.0 micrograms i.c.v. The results of the present study indicate that differences in brain sensitivity of LS and SS mice to ethanol may be mediated by genetic differences in NT systems. Likewise, NT, and probably beta-endorphin, may interact with other neurochemical processes that are involved in the mechanism of ethanol-induced anesthesia and that differ genetically in LS and SS mice.
 ...
PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

The pattern of GH secretion undergoes substantial changes in the aging rat, resulting in decreased daily secretion of GH. In this study, the pituitary responsiveness to GH-releasing factor (GRF) was examined in young (2- to 5-month old) and aging (14- to 18-month old) male rats. In vivo studies were performed under sodium pentobarbital anesthesia. After injection of 250 ng GRF/100 g BW, young rats experienced more GH secretion [peak level, 544.5 +/- 209.5 (+/- SEM) ng/ml] than did 18-month-old rats (89.3 +/- 13.7 ng/ml). To investigate the locus of this insensitivity to GRF, anterior pituitary cells from young and aging rats were dispersed and placed in primary culture. While basal GH secretion from the cultured pituitary cells was similar in the two groups (49.7 +/- 3.5 vs. 47.8 +/- 2.7 ng/ml X 4 h for the 2- and 18-month old rats, respectively), the GH-releasing ability of GRF was partially but significantly impaired in cells derived from both 14- and 18-month old rats; 100 nM GRF stimulated the release of 96.7 +/- 1.8 ng/ml X 4 h in the 18-month old rats as opposed to 115.0 +/- 6.0 (P less than 0.05) ng/ml X 4 h in the 2-month-old rats. Since GRF stimulates GH release through the activation of adenylate cyclase, intracellular cAMP levels were measured in the cultured pituitary cells. GRF stimulated 65% less intracellular cAMP accumulation in the 18-month-old rats. In 14-month-old rats, the ability of forskolin and (Bu)2 cAMP to release GH was impaired, while phorbol ester-elicited GH secretion was unchanged. In conclusion, the GH response to GRF is blunted in aging rats. While much of the insensitivity to GRF may be mediated by the increased somatostatin tone reported in aging rats, a diminished pituitary cAMP response to GRF may also be an important etiological factor in the hyposomatotropinemia of the aging male rat.
 ...
PMID:Diminished pituitary responsiveness to growth hormone-releasing factor in aging male rats. 300 51

To investigate the neural mechanism involved in suppression of GH secretion, we examined the effect of electrical stimulation of the midbrain central gray (CG) and several raphe nuclei on human (h) GRF-induced GH secretion in pentobarbital-anesthetized rats. A concentric bipolar stimulating electrode was implanted stereotaxically into each nucleus under pentobarbital anesthesia 1 week before stimulation. Blood samples were taken through a cannula placed in the right atrium via the right external jugular vein. Under pentobarbital anesthesia, 5 micrograms hGRF dissolved in 0.3 ml saline were systemically applied through this cannula. Ten minutes after the infusion, plasma GH was increased from the resting value of 28.5 +/- 7.1 ng/ml (mean +/- SE) to 686.1 +/- 62.0 ng/ml. Biphasic electrical stimulation was delivered for the first 10 min. When the CG was stimulated with a current of 500 microA, hGRF-induced GH secretion was markedly suppressed. However, even when the stimulation site was outside the CG, hGRF-induced GH secretion was suppressed. But with a smaller current (100 microA) the suppressive effect was observed only when the medial portion of the CG was stimulated. This suppression was abolished by prior lesioning of the hypothalamic periventricular nucleus (Pe), in which most of the somatostatin-immunoreactive fibers in the median eminence originate. The stimulation of the dorsal raphe with a current of 500 microA suppressed the GH increment at 10 min, but no suppression occurred with a current of 100 microA. This suppression was abolished by prior lesioning of the Pe. Electrical stimulation of the rest of the raphe nuclei had no effect on hGRF-induced GH secretion. These results suggest that electrical stimulation of the CG suppresses hGRF-induced GH secretion, and the most effective area is the ventromedial portion of the CG. These suppressive actions may be achieved by activation of the somatostatin neurons in the Pe.
 ...
PMID:Suppression of human growth hormone (GH)-releasing hormone-induced GH secretion in pentobarbital-anesthetized rats after electrical stimulation of the midbrain central gray and several raphe nuclei. 312 2

Evident progress has been made in the treatment of pheochromocytoma. The results of hormone analysis became very accurate, the method for tumor localisation are non invasive and safe: with 131-I-MIBG, ultrasonography and CT-scan an exact preoperative localisation is possible without serious risks. Patients are prepared for the operation with alpha- and beta-blocking agents. Modern methods of anaesthesia with continuous monitoring of blood pressure, pulmonary pressure and cardiac output and a standardized operative procedure are essential. From 1965 to 1987 71 patients with a total of 87 catecholamine producing tumors have been operated. In all cases a transabdominal access was chosen. Biadrenal tumors were removed in 8 patients, multiple (7) tumors in 2 patients. The comparison of the 2 time intervals 1965 to 1976 and 1977 to 1987 showed a significant decrease of serious intra- and postoperative complications. Surgical specimens of 36 patients with pheochromocytoma were used for immunohistologic evaluation. Marked positivity was found in 44% of cases for calcitonin. The reaction for vasoactive intestinal polypeptide (VIP) was positive in 28% of cases. Somatostatin was not detected in any case, neuron-specific enolase (NSE) in all cases. 6 patients with malignant pheochromocytoma were treated with high doses of 131-I-MIBG, 4 other patients received a combined chemotherapy.
 ...
PMID:[Treatment of pheochromocytoma: changes in diagnosis and therapy]. 321 83

Computerized gas chromatography-mass spectrometry was used to measure precisely the hypothalamic levels of noradrenaline (NA), dopamine and serotonin together with those of their major neuronal metabolites 3,4-dihydroxyphenylethyleneglycol (DHPG), 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid in normal male rats 45 min after stimulation of hypothalamic-pituitary-adrenal function by urethane (1.3 g/kg) administration. Urethane treatment resulted in a significant elevation of central noradrenergic neuronal activity (NNA) as assessed from marked rises in hypothalamic DHPG concentrations and the ratio (DHPG/NA). At the same time there was significant stimulation of ACTH and corticosterone release and inhibition of growth hormone release. These hormonal and central effects of urethane (but not anesthesia) were inhibited when the alpha 2-agonist clonidine (150 micrograms/kg) was co-administered. Urethane had no major effect on hypothalamic dopamine or serotonin status. We propose that the release of ACTH and the suppression of growth hormone release following urethane anaesthesia is a result of activation of central NNA and suggest that the hormonal responses are mediated via hypothalamic noradrenergic facilitation of corticotrophin releasing factor and somatostatin release to the anterior pituitary.
 ...
PMID:Stimulation of the hypothalamic-pituitary-adrenal axis and inhibition of growth hormone release via increased central noradrenaline neuronal activity by urethane anaesthesia in the rat: blockade by clonidine. 327 55

Somatostatin was administered intravenously to male Wistar rats, recovered for 3 h from an anesthesia during which the common bile duct and jugular vein were cannulated. Different bile acid-secretory rates were obtained by infusion of saline, or of Na+-taurocholate (150 nmol/min/100 g body wt), or by 8-h bile depletion. At the dose of 2 micrograms/h/100 g body wt, somatostatin causes a prompt decrease of bile flow (about 30%) and of bile acid secretion (32%-47%). The bile acid-independent fraction of canalicular bile is more decreased than the one associated with bile acid secretion. The changes are dose dependent and show a saturation pattern, with half-maximal saturation already at 2.2 ng/min/100 g body wt. Despite this cholestasis, endogenous bilirubin secretion remained unchanged, pointing to different secretory mechanisms for bilirubin and bile acids. In the isolated and perfused liver, somatostatin displays an anticholeretic effect, proportional to the amount of Na+-taurocholate present in the system. Hepatic blood flow and O2 consumption remained constant during perfusion, and were not affected by somatostatin. The hepatic transport of bile acid, and the water and electrolyte secretion are directly affected by somatostatin, and the experimentally-induced cholestasis seems a new and suitable model for studying mechanisms of bile secretion.
 ...
PMID:Cholestatic action of somatostatin in the rat: effect on the different fractions of bile secretion. 611 14

Administration of cysteamine (mercaptoethylamine) induces in rats severe perforating duodenal ulcers. Because the ulcerogenic properties of cysteamine are markedly reduced by treatment with somatostatin, we considered the possibility that cysteamine-induced duodenal ulcer might be mediated by depletion of tissue somatostatin, and thereby of its paracrine influences on gastrin and gastric acid secretion. To test this hypothesis, we measured the concentration of immunoreactive somatostatin (IR-somatostatin) in stomach and duodenal mucosa at intervals after administration of a single ulcerogenic dose (30 mg/kg by stomach tube). IR-somatostatin in these tissues fell rapidly to reach a minimum at 4 h (stomach 31%, duodenum 60% of control respectively). IR-somatostatin in hypothalamus and pancreas decreased gradually to a minimum at 7 h. Another duodenal ulcerogen, propionitrile (10 mg/100 g bw, s.c.) which is more toxic than cysteamine, and several stressful procedures including ether anesthesia, restraint and s.c. formalin did not lower stomach or duodenal IR-somatostatin. Gut, pancreas and hypothalamic VIP levels were not influenced by cysteamine. These findings suggest that cysteamine is a relatively specific depletor of tissue somatostatin. Because blood levels of somatostatin fell, and only trivial amounts of the peptide were found in the stomach lumen after cysteamine administration, it appears likely that this agent acts at the cellular level to cause breakdown of preformed somatostatin and/or to acutely reduce its synthesis.
 ...
PMID:Somatostatin in rat tissues is depleted by cysteamine administration. 611 61

Responses of 291 neurons to microelectrophoretically injected somatostatin were studied in the amygdala of rabbits under nembutal anesthesia. Both excitatory and inhibitory effects were found in contrast to earlier data on the only inhibitory reactions in hypothalamic neurons. After partial chronical deafferentation of the amygdala responses to somatostatin application were observed in 76% of the registered neurons, 90% of these neurons with background discharge frequency from 6 to 20 imp/s, responded by an increase in their activity, while inhibitory reactions were recorded in neurons with average background discharge frequency above 20 imp/s. Since amygdaloid neurons exert a regulating effect on the secretion of the growth hormone through somatostatin, it is suggested that the observed responses reflect one of their feedback mechanisms.
 ...
PMID:[Effect of somatostatin on neurons of partially deafferented amygdala in the rabbit]. 613 Apr 82

A steady maximal biliary secretion of bilirubin has been produced in male Wistar rats, recovered from anesthesia, by continuous infusion of 256 nmol of unconjugated bilirubin per hour per 100 gm body weight, after priming with 3.4 mumols. The administration of somatostatin (2 micrograms/hr/100 gm body weight) produced a reversible decrease of bile flow and bile acid excretion while bilirubin output was unchanged. After discontinuation of somatostatin, a slight increase in the output of bilirubin conjugates was observed with the rapid recovery of bile flow. Administration of Na+ taurocholate at increasing rates (30 to 480 nmol/min/100 gm body weight) progressively enhanced bile flow and bile acid secretion. The rate of secretion of bilirubin conjugates increased to 18% above the values in controls at a taurocholate dose of 120 nmol/min/100 gm body weight and remained at that level with higher amounts, in spite of further increases in flow. Under Na+ taurocholate, somatostatin failed to reverse the enhancement of bilirubin output, although it still inhibited the secretion of bile acids and bile flow. A mechanism linked to osmotic flow induced by taurocholate would appear to serve as a component of the total capacity of the hepatocyte to transfer bilirubin conjugates into the canaliculus. At low bile-acid secretory rates this component seems of minor quantitative importance, whereas a major (specific) pathway seems not yet saturated.
 ...
PMID:Maximal hepatic bilirubin transport in the rat during somatostatin-induced cholestasis and taurocholate-choleresis. 613


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>