Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic injections of cholecystokinin octapeptide sulfate ester (CCK-8-SE) elicit various behavioral and autonomic responses, such as increases in nonrapid-eye-movement sleep (NREMS) and hypothermia. There are two CCK receptors; both CCK-A and CCK-B receptors are stimulated by CCK-8-SE. The relative importance of the CCK-A and CCK-B receptors in the somnogenic and hypothermic effects of CCK-8-SE is not well understood. In the present experiments, we studied the effects of the selective activation of CCK-B receptors by CCK tetrapeptide (CCK-4) or nonsulfated CCK-8 (CCK-8-NS) on sleep and brain temperature (Tbr). Rats were injected intraperitoneally with saline on the control day and with CCK-8-NS (10, 50, or 250 microg/kg) or CCK-4 (10, 50, or 250 microg/kg) on the test day 5-10 min before dark onset. Electroencephalogram, electromyogram, and Tbr were recorded for 12 h. None of the treatments affected sleep or Tbr significantly, with the exception of 10 microg/kg CCK-4, which transiently decreased the amount of NREMS, and 10 microg/kg CCK-8-NS, which slightly increased REMS. These results suggest that the activation of CCK-B receptors by systemic injection of CCK-4 or CCK-8-NS is not sufficient to elicit increased NREMS and hypothermia in rats.
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PMID:Selective activation of CCK-B receptors does not induce sleep and does not affect EEG slow-wave activity and brain temperature in rats. 922 59

The effects of cholecystokinin-8 sulfate (CCK-8), cholecystokinin-8 unsulfate (CCK-8U), cholecystokinin-4 (CCK-4), caerulein and morphine on mice core body temperature have been studied in the present work. Subcutaneous injection of different doses of caerulein (0.05, 0.1 and 0.5 mg/kg), CCK-8 (0.05, 0.1 and 0.25 mg/kg) and morphine (10, 20 and 30 mg/kg) induced hypothermia. CCK-8U and CCK-4 did not elicit any response. The hypothermic response induced by caerulein, a CCK-related decapeptide but not morphine was decreased by selective CCK(A) receptor antagonist MK-329. However, the hypothermia induced by morphine but not caerulein was reduced by opioid antagonist naloxone. When morphine plus caerulein was administered a higher hypothermia was induced. Pretreatment of animals with L-365 260, a selective CCK(B) receptor antagonist did not alter the hypothermia induced by the drugs. The response induced by combination of the both drugs was decreased by MK-329. Administration of CCK antagonists MK-329 and L-365 260 to mice did not exert any effect on temperature. It is concluded that the CCK(A) receptor mechanism may be involved in the hypothermic effect of CCK agonists or morphine, while opioid receptor mechanism is not involved in CCK receptor agonists' response.
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PMID:Cholecystokinin and morphine-induced hypothermia. 1020 91

Previous studies suggested that peripheral immune mediators may involve intermediates acting on the vagus nerve, such as CCK or serotonin (5-HT). We have therefore investigated a possible role for vagal CCK-A and 5-HT(3) receptors in the febrile response after intraperitoneal human recombinant interleukin-1beta (IL-1beta) or lipopolysaccharide (LPS). Unanesthetized, adult male rats instrumented with abdominal thermistors were given intraperitoneal CCK-8 sulfate (100 or 150 microgram/kg) or 2-methyl-5-hydroxytryptamine maleate (4 mg/kg). In other experiments, rats were treated with either antagonists to the 5-HT(3) receptor (ondansetron HCl; 100 microgram/kg) or the CCK-A receptor (L-364,718, 100 or 200 microgram/kg) in combination with LPS or IL-1beta. CCK administration caused a short-lived hypothermia, but interference with the action of endogenous CCK at CCK-A receptors was without effect on IL-1beta- or LPS-induced fever. Neither activation of 5-HT(3) receptors nor blockade of 5-HT(3) receptors affected body temperature or LPS fever. Taken together, our data support the idea that vagal afferents responsive to pyrogenic cytokines may be different from those responsive to CCK or 5-HT.
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PMID:Vagal CCK and 5-HT(3) receptors are unlikely to mediate LPS or IL-1beta-induced fever. 1095 54


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