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)

Neuropeptide Y (0.24 and 1.17 nmol icv) and clonidine (0.025, 0.05 and 0.1 mg/Kg ip) induced a slight decrease of short duration of the rectal temperature in mice in a dose-dependent manner. While pretreatment with yohimbine (0.5 mg/Kg sc), was without effect on neuropeptide Y-induced hypothermia, it attenuated the hypothermic effect of clonidine. The association of neuropeptide Y (0.05 and 0.24 nmol icv) with clonidine (0.0125, 0.025, 0.05 and 0.1 mg/Kg ip) induced a synergistic effect, but it only was significant when neuropeptide Y 0.05 and 0.24 nmol icv was associated with clonidine 0.1 mg/Kg ip and when neuropeptide Y 0.05 nmol icv was associated with clonidine 0.05 mg/Kg ip. These results suggest that the effect of neuropeptide Y is not mediated by an interaction on alpha 2-adrenoceptor, but in accordance with these results, the existence of a collaborative mechanism between both neuropeptide Yergic and noradrenergic systems cannot be ruled out.
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PMID:Central administration of neuropeptide Y induces hypothermia in mice. Possible interaction with central noradrenergic systems. 260 85

Experiments on cats revealed an emotiotropic action of melanostatin on the original spectrum of emotional reactivity, similar to the effects of L-DOPA and amantadin. The drug does not possess an antidepressant action proper but activates the aggressive-defensive behaviour in experimental reserpine depression and reduces the provocation-induced aggressive behaviour in experimental haloperidol depression. In reserpinized mice, it antagonizes reserpine hypothermia, increases muscle tone and eliminates ptosis. It decreases haloperidol-induced catalepsia. Melanostatin increases the brain level of dopamine and its metabolite, homovanilic acid.
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PMID:[Psychopharmacologic spectrum of melanostatin]. 610 96

Neuropeptide Y (NPY) is a highly potent endogenous peptide which when injected into the medial hypothalamus causes spontaneous eating behaviour and an intense fall in body temperature (Tb). This study used antisense oligodeoxynucleotides (ODNs) to determine whether the Y1 subtype of NPY receptor could underlie these remarkable physiological responses. In the unrestrained rat, the ventromedial hypothalamus (VMH) which is highly reactive to NPY was injected with antisense for NPY (aNPY), Y1 receptors (aNPY-Y1) and mismatched controls (mNPY; mNPY-Y1). After cannulae were implanted bilaterally in the brain of 19 rats, 0.4 or 0.8 microgram per 0.8 microliter of the phosphorothioate synthesised ODNs were delivered to the VMH of the rats at 12 h intervals over 2 d. Only the lower dose of aNPY-Y1, but not aNPY, evoked an intense phasic rise in the Tb following each micro-injection. Simultaneously, 0.4 microgram per 0.8 microliter of aNPY-Y1, but not aNPY, suppressed feeding behaviour after a sequence of micro-injections and on the following day. Body weights and locomotor activity of the rats likewise declined concomitantly with the hyperthermia and hypophagia caused by the Y1 receptor antisense. Neither of the control ODNs for NPY or Y1 receptors injected similarly in the VMH of the rats exerted any effects on these measures. These results clearly provide convincing evidence that in the VMH the Y1 subtype of NPY receptor mediates, in part, the neuronal mechanisms responsible for spontaneous feeding and hypothermia produced by native NPY when applied directly to this structure. The concurrent decline in body weight and activity caused by aNPY-Y1 could be caused by the episodes of hyperthermia.
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PMID:Antisense to NPY-Y1 demonstrates that Y1 receptors in the hypothalamus underlie NPY hypothermia and feeding in rats. 876 Apr 91

Orexin A and neuropeptide Y that are known to induce a feeding response when applied centrally, in the present studies also caused hypothermia. Neuropeptide Y elicited hypothermia by depressing metabolic rate (without affecting heat loss mechanisms), while orexin A acted through enhancing peripheral heat loss (without affecting metabolic rate). Neither peptide induced coordinated thermoregulatory changes, both of them appeared to influence thermoregulation via different effector mechanisms.
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PMID:Central thermoregulatory effects of neuropeptide Y and orexin A in rats. 1094 51

The on-going high mortality from sepsis motivates continuous research for novel therapeutic strategies. Neuropeptide Y (NPY), a sympathetic neurotransmitter, has been shown to increase survival in experimental septic shock in rats. This protective effect might be due to immunological, cardiovascular or thermoregulatory effects. The aim of this study was to examine the in vivo effect of peripherally administered NPY on body temperature, blood pressure and heart rate in endotoxaemic animals. In order to obtain clinically relevant data, various physiological parameters were monitored in parallel via radio-telemetry in chronically intravenously cannulated, freely behaving rats. Rats received a sublethal bolus of lipopolysaccharide (LPS, 100 microg kg(-1) I.V.) and the three parameters were continuously recorded for 72 h. Endotoxaemic rats showed a long-lasting hypotension, an initial hypothermia (-0.5 degrees C), followed by a prolonged febrile phase (+1.6 degrees C 6 h after endotoxin challenge) associated with a decrease of the circadian rhythm amplitude of temperature. Pretreatment with NPY (160 pmol kg(-1) I.V. over 75 min) prevented hypotension and significantly stabilized body temperature immediately following the application. The febrile phase was effectively reduced for at least 72 h. These telemetrically obtained findings clearly demonstrate that pretreatment with NPY positively influences two life-threatening symptoms in endotoxaemia and might be a future option for a successful clinical treatment regimen.
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PMID:Neuropeptide Y stabilizes body temperature and prevents hypotension in endotoxaemic rats. 1538 81