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)

Cholecystokinin-octapeptide (CCK-8) was shown to cause hypothermia after intracerebroventricular administration in the rat, and the hypothermic effect of CCK-8 was antagonized by simultaneous injection of TRH.
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PMID:Cholecystokinin-induced hypothermia in the rat. 625 73

Cholecystokinin octapeptide (CCK-8), ceruletide (caerulein, CER) and 10 analogues of ceruletide, were studied in mice for antagonism of the tremors induced by harmine (5 mg/kg, s.c.), ibogaine (20 mg/kg, s.c.) and oxotremorine (0.2 mg/kg, s.c.). The following reference drugs were tested for comparison: prolyl-leucylglycine amide (MIF), atropine, haloperidol, biperiden, ethopropazine, trihexyphenidyl, methixene and clonazepam. All treatments were subcutaneous, the antagonists being given 10 min (in some trials 30 min) before the tremorogen. Tremorolytic potency (ED50) was calculated from dose-response curves. Against the tremors induced by either harmine or ibogaine, CCK-8 and ceruletide, as well as many of the analogues of ceruletide had greater tremorolytic potency than the reference drugs. Against oxotremorine, however, ceruletide and its most potent analogue, Nle8-CER (other analogues were not tested) were inactive and MIF showed very little effectiveness. Additional experiments on hypothermia and sedation as well as evaluation of previous studies on other central actions suggested that the tremorolytic effect of CCK-like peptides is independent of other central effects. The CCK-like peptides may play a physiological role in the regulation of extrapyramidal motor activity.
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PMID:Cholecystokinin octapeptide (CCK-8), ceruletide and analogues of ceruletide: effects on tremors induced by oxotremorine, harmine and ibogaine. A comparison with prolyl-leucylglycine amide (MIF), anti-Parkinsonian drugs and clonazepam. 631 Apr 34

The C-terminal octapeptide of cholecystokinin (CCK-8) injected into the lateral ventricle of rats produced a lowering of body temperature. CCK-8 potentiated pentobarbital-induced hypothermia, but not the ethanol one. Thyrotropin releasing hormone (TRH) and prostaglandin E2 (PGE2) antagonized the hypothermic effect of CCK-8. Non-sulfated CCK-8 was ineffective in lowering body temperature, indicating that sulfated tyrosine in the CCK molecule is indispensable for its hypothermic action. Caerulein was found to possess rather less activity compared with CCK-8.
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PMID:Effect of cholecystokinin octapeptide on body temperature in the rat. 680 79

Sixteen peptides were injected intracerebroventricularly to test their effects on rectal temperature of rabbits in a thermoneutral environment. In initial tests 5 micrograms alpha-MSH, ACTH(1--24), oxytocin, vasopressin and glucagon altered body temperature while ACTH(1--10), cholecystokinin, contraceptive tetrapeptide, gastrin, insulin, interferon, leupeptin, LHRH, panhibin (somatostatin), and proctolin did not. Bombesin also altered body temperature but in no consistent direction. In further tests on the effective peptides 1.25--5.0 micrograms alpha-MSH and ACTH(1--24) produced dose-related decreases in rectal temperature as great as 1.0 degrees C. The same doses of oxytocin and glucagon produced small, prolonged hyperthermias which did not exceed 0.4 degrees C. Vasopressin caused rapid development of small increases in rectal temperature; temperature returned to normal in 2--3 hr. The results suggest that five of the peptides tested may have roles in central mediation of normal body temperature, hypothermia, hyperthermia and fever.
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PMID:Central administration of peptides alters thermoregulation in the rabbit. 724 7

We examined the effects of intracerebroventricular (i.c.v.) injections of cholecystokinin-octapeptide (CCK-8) and somatostatin (SST) and the interactions of these neuropeptides with the selective opioid antagonists, CTAP (mu) and nor-BNI (kappa) and the mu-agonist, PL017, on body temperature (Tb) of the rat at normal ambient temperature (21 +/- 0.5 degrees C). CCK-8 produced short-lasting (15-60 min), dose-related increases in Tb in a dose range of 20 to 900 ng but did not change the Tb at lower doses (0.1-2 ng). Lower doses of SST (1 and 2 micrograms) produced hyperthermia (30-60 min) and a higher dose of SST (10 micrograms) caused hypothermia (30-45 min). PL017 (1 microgram, i.c.v.), alone and in combination with CCK-8, produced hyperthermia. The CCK-8 (300 ng)-induced hyperthermia was blocked by pretreatment of rats with CTAP (1 microgram, i.c.v.), suggesting that the higher doses of CCK-8 increase Tb through the interaction with mu-receptors or the enhancement of release of endogenous opioids acting on the mu-receptor. The hyperthermia elicited by a lower dose of SST (1 microgram) was prevented by pretreatment with CTAP but not with nor-BNI (1 microgram, i.c.v.). Pretreatment with nor-BNI blocked the higher dose (10 micrograms) of SST-induced hypothermia. PL017 or CTAP did not prevent the hypothermic effect of that dose of SST. These results indicate that a lower dose of SST (1 microgram) stimulates the mu-receptor (directly or indirectly) and a higher dose (10 micrograms) interacts with the kappa-receptor in regulation of Tb. Thus, the effects of both CCK-8 and SST on Tb appear to involve the endogenous opioid system.
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PMID:Interaction of cholecystokinin and somatostatin with a selective mu-opioid agonist and mu- and kappa-antagonists in thermoregulation. 903 4

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

The vagus nerve may indirectly influence thermoregulation by modulation of energy balance: its afferent fibers convey signals that represent information on feeding state, resulting in either depression or stimulation of metabolic processes. A regulated metabolic depression can be detected in the background of fasting-induced hypometabolism and hypothermia. In its development (besides humoral signals) vagally transmitted neural signals of gastrointestinal and hepatoportal origin are important. These signals are related to hunger, to decrease of mechanical/chemical stimuli from the gut, to decline of blood glucose; they alter discharge rates of vagal afferents and activity of the nucleus of the solitary tract, eliciting inhibition of metabolic rate and enhancement of food intake. In this hunger-related metabolic inhibition the nucleus of the solitary tract is in interaction with hypothalamic nuclei, that contribute to neuropeptide changes characterized by high neuropeptide Y activity (with energy-conserving type of regulation) and depressed cholecystokinin and corticotropin releasing hormone activities (with depressed energy-expenditure). In postalimentary states the hypermetabolism and hyperthermia are due to opposite changes in metabolic regulation. Satiety-related stimulatory signals of abdominal origin, transmitted via hepatic vagal afferents to the nucleus of the solitary tract, contribute to enhancement of sympathetic activity and stress-responsiveness, leading to hypermetabolism and hyperthermia. Depressed neuropeptide Y release and enhanced cholecystokinin and corticotropin releasing hormone activities participate in the central regulatory changes, and in the high energy-expenditure. The biological role of these vagal functions is not directly the regulation of body temperature, rather the regulation of energy balance and energy content in the body.
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PMID:The vagus nerve in thermoregulation and energy metabolism. 1118 24

The multiple effects of vagotomy on the thermoregulatory response to systemic inflammation are reviewed (primarily, for the model of intravenous lipopolysaccharide administration in the rat). The following conclusions are drawn. (1) Vagotomy-associated thermoeffector insufficiency is likely to account for the attenuation of the fever response observed in some--but not all--studies; such an insufficiency is, however, preventable by postoperative care, including the use of a liquid diet. (2) The febrile response to low doses of lipopolysaccharide (monophasic fever) is mediated by the hepatic (but not gastric or celiac) vagal fibers, presumably afferent; the same fibers are likely to be involved in the development of tolerance to low doses of circulating endotoxins. (3) Phase 1 of the polyphasic febrile response to moderate doses of lipopolysaccharide involves capsaicin-sensitive afferents (either nonvagal only or both nonvagal and vagal), does not involve cholecystokinin A-receptors, and may involve peripheral prostaglandins. (4) Febrile phase 2 does not require the integrity of abdominal nerve fibers, either vagal or nonvagal, at least in the rat. (5) Phase 3 of the febrile response to intravenous lipopolysaccharide (and perhaps the response to intraperitoneal lipopolysaccharide) involves capsaicin-insensitive vagal fibers, presumably efferent; the involvement of these fibers in febrigenic mechanisms is strongly modulated by an unknown factor. (6) A hepatoceliac vagal, presumably efferent, mechanism ('an anti-inflammatory pathway') counteracts the development of lipopolysaccharide-induced hypothermia and shock.
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PMID:Thermoregulatory manifestations of systemic inflammation: lessons from vagotomy. 1118 25

Thermoregulatory effects of cholecystokinin (CCK) peptides are reviewed with special emphasis on two types of responses, that is hypothermia or hyperthermia. In rodents exposed to cold a dose-dependent hypothermia has been observed on peripheral injection of CCK probably acting on CCKA receptors. Central microinjection of CCK in rats induced a thermogenic response that could be attenuated by CCKB receptor antagonists, but some authors observed a hypothermia. It is suggested that neuronal CCK may have a specific role in the development of hyperthermia, and endogenous CCK-ergic mechanisms could contribute to the mediation of fever. Possible connections between thermoregulatory and other autonomic functional changes induced by CCK are discussed.
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PMID:Cholecystokinin and thermoregulation--a minireview. 1145 17


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