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)

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

An intracisternal injection of somatostatin-28 produced hyperthermia in rats at cold, thermoneutral, warm ambient temperatures. The hyperthermic response to somatostatin-28 was not prevented by pretreatment of rats with the following agents: alpha-methylparatyrosine, phenoxybenzamine, propranolol, sulpiride, atropine, methysergide or naloxone. Somatostatin-28 prevented hypothermia induced by bombesin and gamma-MSH when it was administered simultaneously, but it left the hyperthermic response to TRH intact. The results indicate that somatostatin-28 produces hyperthermia by elevating a "set point" or regulated level of temperature. Under the conditions tested, the hyperthermic response to somatostatin-28 does not appear to be dependent on muscarinic cholinergic, serotonergic, alpha- or beta-adrenergic, dopaminergic or endogenous opiate system.
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PMID:Hyperthermic action of somatostatin-28. 613 57

The pharmacology and neurochemistry of bombesin-like peptides was investigated. Synthetic analogues which had modifications near the N-terminal inhibited specific binding of (125I-Tyr4)BN with high affinity in rat brain and these peptides were potent hypothermic agents after central injection. In comparison, BN-like peptides with modifications near the C-terminal bound with low affinity and were not potent hypothermic agents. These data indicate that the C-terminal of BN is required for central high affinity binding and biological potency. Because substitution of D for L-amino acids at the 8, 10, 13 or 14 positions greatly reduced receptor binding affinity and ability to induce hypothermia, central receptors for BN show marked stereospecificity. Also, the pharmacology of BN in the periphery was investigated using dispersed guinea pig pancreatic acini and found to be similar to that of the brain. Because endogenous BN-like peptides extracted from brain tissue possess appreciable biological activity, these receptors are likely activated by endogenous BN-like peptides in vivo.
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PMID:Pharmacology and neurochemistry of bombesin-like peptides. 618 94

The ability of substance P analogues to inhibit the action of bombesin in the CNS was investigated using receptor binding and biological assays. The putative substance P antagonists inhibited binding to central receptors for both substance P and bombesin-like peptides. Spantide, which was the most potent analogue tested, reversed the bombesin induced hypothermia and grooming. Therefore the putative substance P antagonists may also antagonize the actions of bombesin in the CNS.
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PMID:The antagonism of bombesin in the CNS by substance P analogues. 620 51

The effects of the three peptides neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors were studied in mice. Intracisternal administration of these peptides to mice prolonged the duration of sleep induced by ethanol (5.2 g/kg). Neurotensin and beta-endorphin also enhanced ethanol-induced hypothermia. None of the peptides, when administered alone, produced sleep. However, all three compounds impaired the aerial righting reflex and induced sleep when followed by an IP dose of ethanol (3.5 g/kg), which alone did not induce sleep. These results, taken together with previous findings, suggest that neuropeptides may be involved in the complex mechanisms of action of ethanol on the CNS.
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PMID:The effects of neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors in mice. 630 2

Neurotensin and bombesin have been tested for their effects on body temperature and locomotor activity in an open field. Both peptides induce hypothermia and suppress ambulation and rearing. The time curves of the hypothermic effects of both peptides appear to be rather similar, although bombesin is a more potent hypothermic agent than neurotensin. The time curves of the effects on locomotor activity appear to be quite different. The suppressive effect of neurotensin on locomotor activity is relatively short lasting and reaches its maximum at approximately 32 minutes. The effect of bombesin follows a different time curve and shows two peaks, suggesting that two different mechanisms are involved in the suppressive action of bombesin on locomotor activity. Calculation of the correlation coefficients between the effects of neurotensin and of bombesin on body temperature and on locomotor activity (ambulation) suggest that a causal relationship between these two effects is not likely, in particular for neurotensin.
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PMID:Neurotensin and bombesin, a relationship between their effects on body temperature and locomotor activity? 648 31

Hypothermia and hypophagia have been elicited, under a variety of experimental conditions, by central injections of bombesin. The preoptic area of the anterior hypothalamus has been suggested as the active site for the hypothermia observed in rats exposed to cold, while the lateral hypothalamus has been implicated in the production of hypophagia induced by bombesin. Data are reported here demonstrating a significant, dose-related decrease in both intake of food and body temperature following microinjections of bombesin into the substantia nigra of male rats deprived of food for 18 hr. Similar injections into the preoptic area, the lateral hypothalamus and the ventromedial hypothalamus failed to produce a consistent decrease in either intake of food or body temperature. Although a decrease in body temperature was demonstrated following injections into the paraventricular nucleus of the hypothalamus, this decrease did not appear to be dose-related. Injections of bombesin at this site had no effect on food intake. The possibility of an underlying dopaminergic mechanism for the hypothermic and hypophagic effects of bombesin is discussed.
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PMID:Injections of bombesin into the substantia nigra produce hypothermia and hypophagia in food-deprived rats. 652 54

The present study measured oxygen consumption and core body temperature following central injections of bombesin (1.0 microgram) in food-deprived rats. Oxygen consumption did not differ for bombesin- and control-injected rats while mean core body temperature decreased significantly following bombesin administrations. Present findings suggest separate mechanisms of heat loss for bombesin-induced hypothermia in cold-exposed and food-deprived rats.
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PMID:Effects of bombesin on body temperature and oxygen consumption in food-deprived rats. 652 40

Bombesin is an oligopeptide which has been implicated as a possible neurotransmitter or neuromodulator in the central nervous system. Central administration of the peptide produces physiological and behavioral responses which suggest a downward shift in the set point of body temperature. These include hypothermia, decreased metabolic rate and increased behavioral responding to escape from radiant heat. Contradictory data also exist. Therefore, a series of experiments was conducted to evaluate further the effects of the central administration of bombesin on behavioral thermoregulation and general locomotor activity. It was found that microinjections of bombesin into the preoptic area of the anterior hypothalamus increased the number of behavioral responses to radiant heat. The increased responding for heat-reinforcement and heat-escape suggested an activation of general locomotor activity. This was confirmed by the finding that centrally-administered bombesin increased the number of responses to escape from radiant heat without altering the duration of exposure to heat. Additionally, bombesin had no effect on the number of heat-escape responses following adrenalectomy. It was concluded that bombesin acts within the hypothalamus to increase general locomotor activity via the sympathetic outflow to the adrenals. This behavioral excitation is apparently expressed as an increase in responding to heat, or escape from heat, independent of thermoregulatory mechanisms. Therefore, the behavioral data do not indicate that bombesin decreases the set point of body temperature.
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PMID:Effects of centrally-administered bombesin and adrenalectomy on behavioral thermoregulation and locomotor activity. 666 58

Intracerebroventricular administration of bombesin, a naturally-occurring peptide, produces hypothermia in the rat. To determine whether a pituitary-dependent step is necessary for this effect, the thermoregulatory response was followed in hypophysectomized and intact rats maintained at room temperature. Significant hypothermia was produced in both experimental groups. This study supports an extra-pituitary mechanism for bombesin-induced hypothermia.
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PMID:Bombesin produces hypothermia in hypophysectomized rats. 685 53


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