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)

The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.
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PMID:Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. 29 52

Thyrotropin-releasing hormone (TRH) was found to antagonize pentobarbital-induced sleeping time and hypothermia. While 3 to 100 mg/kg of TRH reduced pentobarbital sleeping time when administered prior to the barbiturate, a dose-response relationship to TRH could not be established. However, doses of 10 to 100 mg/kg of TRH enhanced the lethality of pentobarbital when these compounds were administered simultaneously. Thyrotropin or L-triiodothyronine did not imitate and hypophysectomy did not reduce the effects of TRH, indicating that the pituitary is not essential for its antagonism of pentobarbital. Studies of TRH analogs provided further support of this view. In addition, TRH reduced the sleep and hypothermia produced by thiopental, amobarbital, secobarbital and phenobarbital, and it antagonized the hypothermia and reduced motor activity produced by chloral hydrate, reserpine, chlorpromazine and diazepam. Intracisternally administered TRH also reduced pentobarbital sleeping time and hypothermia, but melanocyte-stimulating hormone release-inhibiting factor and somatostatin administered by this route did not. While reduction of pentobarbital sleeping time by TRH could not be attributed to an affect on monoamine systems or to deamidated TRH, this action was reduced by intracisternally administered atropine, suggesting that cholinergic mechanisms may contribute to the effects of TRH. Thus, the results provide evidence that TRH acts on brain independent of an effect on the pituitary.
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PMID:Effects of thyrotropin-releasing hormone (TRH) on the actions of pentobarbital and other centrally acting drugs. 80 36

The changes in thermoregulatory effectors produced by an injection of polyriboinosinic acid: polyribocytidylic acid (Poly I:C) or interferon were assessed and compared in control rats, in rats with hypothalamic somatostatin (SS) receptor blockade and in rats with hypothalamic SS depletion. Intrahypothalamic (i.h., 0.05-0.50 microgram) or intraperitoneal (i.p., 100-600 micrograms) administration of Poly I:C caused a dose-related rise in colon temperature in control rats at all ambient temperatures (Ta) studied. A Poly I:C-induced fever was produced by increased metabolism at a Ta of 8 degrees C, whereas at 30 degrees C, it was caused by cutaneous vasoconstriction. At a Ta of 22 degrees C, the fever was caused by increased metabolism and cutaneous vasoconstriction. On the other hand, i.h. administration of SS-14 antagonist (0.1-0.5 ng) caused a dose-related fall in colon temperature at Ta of 8 degrees C or 22 degrees C. At a Ta of 8 degrees C, the hypothermia was caused by decreased metabolism, whereas at 22 degrees C, it was caused by decreased metabolism and cutaneous vasodilation. At a Ta of 30 degrees C, the thermoregulatory effectors were not affected by SS-14 antagonist treatment. Furthermore, the fever induced by Poly I:C or interferon was significantly reduced by pretreatment of rats with an i.p. dose of cysteamine (30 mg. kg-1) or an i.h. dose of SS-14 antagonist (0.1 ng). The results indicate that a somatostatinergic pathway in rat hypothalamus may mediate the fever induced by interferon or its inducer Poly I:C.
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PMID:Febrile effects of polyriboinosinic acid: polyribocytidylic acid and interferon: relationship to somatostatin in rat hypothalamus. 169 81

The changes in both the thermoregulatory responses and brain somatostatin (SS) levels produced by ambient temperature (Ta) changes were assessed in rats after they had been equilibrated to each of the Ta for a period of about 90 min. Cold exposure, in addition to elevating hypothalamic SS-levels, led to increased metabolism and cutaneous vasoconstriction at Ta = 8 degrees C. In contrast, heat exposure, in addition to lowering hypothalamic SS-levels, resulted in decreased metabolism and cutaneous vasodilation at Ta = 30 degrees C. Rats were chronically implanted with a hypothalamic cannula to allow intrahypothalamic injection of SS on the conscious rats. Direct administration of SS (0.1-0.3 micrograms) into the preoptic anterior hypothalamic area caused a dose-related rise in colon temperature at three Ta tested. The SS-induced hyperthermia was produced by increased metabolism at Ta = 8 degrees C, whereas at Ta = 30 degrees C, it was caused by cutaneous vasoconstriction. At Ta = 22 degrees C, the hyperthermia was caused by increased metabolism and cutaneous vasoconstriction. Systemic administration of cysteamine, in addition to lowering hypothalamic SS-levels, produced a dose-related fall in colon temperature at Ta of 8 degrees C and 22 degrees C. The hypothermia induced by cysteamine was produced by decreased metabolism at Ta = 8 degrees C, whereas at Ta = 22 degrees C, it was caused by both decreased metabolism and cutaneous vasodilation. The data indicate that the hypothalamic SS-levels mediate normal body temperature responses in rats.
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PMID:Somatostatin: a hypothalamic transmitter for thermoregulation in rats. 256 82

Somatostatin (SS)-related peptides act within discrete brain regions to inhibit adrenal epinephrine (E) secretion, to prevent hypothermia, and to produce hyperthermia. Depletion of brain concentrations of these SS-related peptides using cysteamine (CSH) or central administration of an SS receptor antagonist increases adrenal E secretion and impairs thermoregulation. These actions of CSH and the SS receptor antagonist are reversed by administration of SS into the central nervous system. These results support the hypothesis that endogenous brain SS-related peptides are involved in the regulation of adrenal E secretion and thermoregulation.
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PMID:Neurobiological actions of cysteamine. 286 18

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.
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PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

Somatostatins, somatostatin-14, somatostatin-28, and desAA [D-Trp8]-somatostatin, with differential potencies, act in the brain to reverse chemical-induced hypothermia and to produce hyperthermia. Somatostatins are more potent and loger acting than prostaglandin E2 in producing hyperthermia. Hyperthermia, induced by somatostatins, is not prevented by previous treatment with the prostaglandin synthesis inhibitor indomethacin. Somtostatins given to obese ob/ob mice prevent development of lethal hypothermia and result in maintenance of euthermia. Continuous infusion of somatostatins results in desensitization to the hyperthermic effects of these peptides. Endogenous somatostatins may be involved in regulation of body temperature.
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PMID:Somatostatin-28, somatostatin-14 and somatostatin analogs: effects on thermoregulation. 611 36

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
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PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11

Bombesin and the somatostatin analog, desAA-[D-Trp8]-somatostatin (ODT8-SS), act within the central nervous system to alter animals' oxygen consumption (VO2) in a manner consistent with the observed effects of these peptides on temperature regulation. Bombesin given intracerebroventricularly (i.c.v.) to rats at cold ambient temperatures prevents elevation of VO2 but does not lower VO2 below the values observed at thermoneutrality. ODT8-SS given i.c.v. increases VO2 of animals at an ambient temperature of 20 degrees C and prevents bombesin inhibition of VO2 at low ambient temperatures. Thus, bombesin inhibits VO2 induced by cold and results in hypothermia, ODT8-SS prevents bombesin-induced inhibition of VO2 and bombesin-induced hypothermia and, ODT8-SS increases VO2 and produces hyperthermia in animals at thermoneutral temperatures.
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PMID:Bombesin and somatostatin related peptides: effects on oxygen consumption. 612 48

The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment on body temperature and serum and tissue levels of thyroid hormones, glucose, glucagon, insulin, and somatostatin were investigated. Within 7 days following TCDD administration (45 micrograms/kg), rats exhibited hypothyroidism compared to pair-fed controls and rats fed ad libitum. Body temperature was maintained in the pair-fed and ad libitum-fed controls but was significantly decreased in TCDD-treated rats at 2 days. Within 2 weeks of the administration of 90 micrograms TCDD/kg, body temperature was below 35 degrees C with the lowest mean value of 34.5 degrees C recorded on Day 16. Mean body temperatures for control rats ranged from 36.8 to 37.5 degrees C. One week after TCDD administration (45 micrograms/kg), serum thyroxine (T4) declined to 46% of pair-fed controls. The decreased free-thyroxine index indicated that the measured decrease in thyroxine reflected decreased hormone concentrations as opposed to altered protein binding. Hypoglycemia occurred in TCDD-treated rats subsequent to hypothyroxinemia and hypothermia, but it did not develop in the pair-fed controls. At 1 week after administration of 45 micrograms TCDD/kg, serum and pancreatic insulin levels were reduced to 25 and 76% of ad libitum-fed controls, respectively. Hypophagia was determined to be responsible for the decreased growth rate and hypoinsulinemia but did not account for hypothyroxinemia, hypothermia, and hypoglycemia following the administration of TCDD. No significant alterations were detected in serum glucagon or in pancreatic, hepatic, or serum somatostatin levels. Decreased somatostatin in the gastric antrum coincided with a 29% increase in stomach dry weight. The delayed toxicity of TCDD may result, in part, from these hormonal alterations.
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PMID:Hypothyroxinemia and hypothermia in rats in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin administration. 613 53


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