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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ACTH (1--24) and alpha-melanotropin (alpha-MSH), peptides previously shown to influence body temperature when administered centrally and to occur naturally in brain regions important to temperature control, were injected intracerebroventricularly (ICV) in rabbits. The peptides in doses of 1.25, 2.5 and 5.0 micrograms produced dose-related hypothermias in a 23 degrees C environment, and greater decreases in body temperature when the experiments were repeated in the cold (10 degrees C), but the largest dose had no effect on temperature in the heat (30 degrees C). These results indicate that the peptides do not reduce the central set-point of temperature control. Rather, they appear to selectively inhibit heat conservation and production responses. Five microgram of ACTH reversed vasoconstriction and inhibited rises in temperature caused by leukocytic pyrogen (LP) given IV and ICV. The same dose of alpha-MSH also reduced fever produced by IV and ICV LP, but the reduction was not as great as after ACTH. Both peptides (5 micrograms) also reduced temperature rises and vasoconstriction caused by ICV PGE2. ACTH reduced d-amphetamine-induced hyperthermia without altering vasoconstriction which suggests that this peptide can reduce temperature rises by inhibiting heat production alone. One of the most important findings was that the peptides are antipyretic in that they reduce fever at doses (0.25 microgram, ICV) that do not affect normal temperature. The powerful effects of these peptides on resting body temperature, hyperthermia and fever, together with their presence in brain tissue important to temperature control, suggest that the endogenous central peptides participate in thermoregulation, perhaps by limiting fever and influencing normal temperature.
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PMID:Hypothermic and antipyretic effects of centrally administered ACTH (1--24) and alpha-melanotropin. 627 Jun 34

Exposure to cold for 2 weeks was used to assess the effects of a sustained stimulus on pituitary-adrenal function in male rats. The diurnal peak in plasma and adrenal corticosterone was advanced by 4 h during the first 24 h of exposure to cold but returned to its usual time (2000 h) by the next day. Plasma ACTH and corticosterone levels were generally greater at all times during the 24-h cycle in animals exposed to cold for up to 2 weeks, with the greatest increase occurring consistently at the time of peak. When rats exposed to cold for 1 week were returned to a normal 24 C environment, plasma corticosterone tended to increase. Plasma ACTH and plasma and adrenal corticosterone responses to a superimposed acute provocative stimulus (ip saline injection) were faster, greater, and more sustained in rats exposed to cold for 3 or 7 days. Similarly, the compensatory adrenal hypertrophy response to unilateral adrenalectomy was greater in cold-exposed rats. Such animals were also more resistant to pituitary-adrenal suppression by prednisolone. In contrast, there was no change in the sensitivity of the adrenal to exogenous ACTH. The results suggest that chronic exposure to cold causes a sustained activation of central mechanisms that regulate pituitary ACTH secretion as well as extra-pituitary mechanisms that regulate adrenal size; it reduces the effectiveness of negative feedback mechanisms, but does not alter those involved in the regulation of adrenal rhythmicity or adrenal sensitivity to ACTH.
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PMID:Pituitary-adrenal function in rats chronically exposed to cold. 627 34

ACTH 1-39 (0.2 U IP daily for up to 18 days) has a beneficial effect on the functional reorganization of regenerating motor units of the extensor digitorum longus (EDL) in the adrenalectomized adult rat following crushing of the peroneal nerve. Motor unit activity (maximum twitch tension amplitude/mean increment in twitch tension as voltage is increased by 0.1 V gradations) and nerve-muscle efficiency (tetanic tension from indirect stimulation/tetanic tension from direct stimulation of EDL) were enhanced by ACTH 1-39. Other electrophysiological and contractile parameters were unaffected by the peptide. Spontaneous motor activity in cold stressed 13 day old rats was prolonged by Org 2766, a substituted analogue of ACTH/MSH 4-9, (0.1 microgram/kg daily) but unaffected by the same dosage of ACTH/MSH 4-10. The responsiveness of developing and regenerating motor systems to neuropeptides indicates a plasticity of neuronal connections, which depends on peptide sequence, dosage and the physiological state of the animal (normal, depressed, regenerating or developing, at rest or stressed).
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PMID:Peptide influences on the development and regeneration of motor performance. 628 82

Plasma levels of immunoreactive ACTH, corticosterone (CS), and PRL in two-kidney, one clip (2K1C) hypertensive SABRA, hypertension-prone (SBH), hypertension-resistant (SBN), and normotensive SABRA rats were compared under both quiescent conditions and after acute (2 min) cold water stress. Serum levels of CS were higher in 2K1C hypertensive compared with normotensive SABRA rats under both quiescent and stressful conditions. Circulating levels of ACTH and PRL were similar in both groups under quiescent conditions. Resting circulating levels of CS were higher in the SBH rats compared with SABRA or SBN rats. Serum PRL levels were similar in SBH and SABRA rats under both quiescent and stressful conditions. Resting PRL levels in the SBN rats were lower compared with the SABRA rats. Resting serum levels of ACTH and CS in the SBN rats were similar to those found in the SABRA rats. After stress exposure serum ACTH and CS levels were elevated in all groups. Serum PRL levels in SBN rats were not affected by stress, unlike the marked elevation seen in the other groups. Our study demonstrates increased secretion of CS in both 2K1C hypertensive and SBH rats under quiescent conditions. Both 2K1C hypertensive and SBH rats have normal hormonal capacity to respond to stress. SBN rats exhibited reduced PRL secretion under both quiescent and stressful conditions. It is suggested that abnormal activity of the hypothalamic-pituitary-adrenal system may play a role in the pathogenesis of 2K1C and genetic hypertension as well as in resistance to hypertension.
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PMID:Stress-induced secretion of adrenocorticotropin, corticosterone, and prolactin in experimentally and genetically hypertensive rats. 629 3

Endorphin and ACTH-like materials levels in rat plasma and pituitary were measured by radioimmunoassay under baseline and cold stress conditions. Cold stress significantly increased plasma beta-endorphin and ACTH immunoreactivity. A rise in these two peptides was also found in the neurointermediate lobe of the pituitary, while in the anterior lobe their levels were unaffected. These findings suggest that the rise of beta-endorphin and ACTH content in the neurointermediate lobe occurs as a compensatory biosynthetic mechanism for the peptides released from the adenohypophysis.
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PMID:Cold stress in the rat induces parallel changes in plasma and pituitary levels of endorphin and ACTH. 629 39

Despite evidence that ACTH release after stress is under excitatory hypothalamic control, a stimulatory role for any of the monoamine neurotransmitters is yet to be clearly demonstrated. In the present investigation computerized gas chromatography/mass spectrometry was used to assess the neuronal activities of hypothalamic dopamine, norepinephrine (NE), and serotonin (5-HT) in rats after stress-induced ACTH release. Medial basal hypothalamic NE neuronal activity as assessed by the ratio of 3,4-dihydroxyphenylethyleneglycol (DHPG) to NE. (DHPG/NE) was elevated (P less than 0.0005) within 2 min after a 3-min cold water swim stress. Ether stress also caused a marked elevation in NE activity (P less than 0.0025). A highly significant positive correlation between the ratio of hypothalamic DHPG/NE and serum corticosterone was found over a large population of normal and stressed rats. Consistent with this relationship between hypothalamic NE neuronal activity and ACTH release being a causal one were the findings that 1) adrenalectomized rats exhibited markedly elevated hypothalamic DHPG/NE ratio and serum ACTH (both P less than 0.0005) together with serum corticosterone levels reduced to about 3% of control levels (P less than 0.0005), and 2) the administration to rats of the alpha-blocker yohimbine or the antianxiety agent diazepam resulted in significant changes in hypothalamic NE activity, together with parallel changes in ACTH secretion. In hypothyroid rats, which have elevated hypothalamic 5-HT activity, and in normal gentled rats, stress caused a significant reduction in hypothalamic 5-HT activity. High hypothalamic activity of dopamine or 5-HT in hypothyroid rats did not significantly affect basal ACTH levels nor prevent the responses to either cold water swim or ether stress, and both stresses resulted in elevated hypothalamic DHPG/NE, serum ACTH, and serum corticosterone (all P less than 0.005) in these animals. From these data it is concluded that NE is an excitatory hypothalamic monoamine for ACTH release in stress and that hypothalamic 5-HT activity is reduced after stress.
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PMID:Hypothalamic monoamine control of stress-induced adrenocorticotropin release in the rat. 630 61

It is concluded that besides NA, some other hormones (adrenaline, glucagon, growth hormone, ACTH, insulin and adrenal steroids) are also thermogenic. While brown adipose tissue is the most important site of heat during NA thermogenesis, some other organs, namely muscles, also contribute to thermogenesis due to various hormones. Hormones seem to potentiate heat production due to their action in target organs. Humoral thermogenesis not only can compensate the heat loss from the body of cold exposed individuals, but it can also prevent obesity under conditions of an high caloric intake. Some substance, on the other hand, induce a hypometabolic effect (rT3, hibernation trigger, antabolone, bombesin). Additionally, absence of gonadal steroids induce hibernation. Thus, humoral substances contribute both to the control of hyper- and hypometabolic states.
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PMID:Humoral control of hyper- and hypometabolic states. 631 84

Analgesia induced in rats by cold-water swim stress and measured by the tail-flick and hot-plate methods was significantly antagonized after IP pretreatment for 3 days with 8 mg/kg dexamethasone. The analgesia developed by the cold-water swim stressor was also attenuated by 1 mg/kg naloxone. These results suggest that the corticosteroids may have a role in modulating stress-induced analgesia and that the adrenal-pituitary axis modulates the endogenous opiate system. These conclusions are based on recent reports that indicate the release of the opiate-like peptide beta-endorphin and adrenocorticotropin (ACTH) from the pituitary are increased by acute stress and inhibited by administration of the synthetic glucocorticoid dexamethasone.
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PMID:Dexamethasone and stress-induced analgesia. 640 29

To test if the adrenocortical axis of the rat loses sensitivity to negative feedback control during aging, we examined corticosterone secretion under basal, stressed and post-stress conditions in young and in aged Fisher male rats. We find no age-related change in the speed or magnitude of the stress response or in the capacity to manifest a corticosterone response following chronic stress. However, we do observe in aging rats an elevation of basal corticosterone and an impaired capacity to adapt to and recover from stress. This latter finding is illustrated by longer latencies relative to young rats, in the return of serum corticosterone concentrations to basal values during sustained exposure to mild cold or following the end of immobilization stress. All of these deficits reflect an increased rate of corticosterone secretion during physiologically inappropriate circumstances. Such observations support the concept that there is an age-related loss of sensitivity of the brain and pituitary to the inhibitory effects of high circulating levels of corticosterone on ACTH release.
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PMID:The adrenocortical stress-response in the aged male rat: impairment of recovery from stress. 668 60

Pregnant female rats were fed either a 5.0-5.5% w/v ethanol-containing liquid diet ad lib or pair-fed the isocaloric control diet during gestation weeks 2 and 3. At 75-105 days of age, female offspring of the ethanol-treated dams showed significantly greater corticosterone responses than pair-fed- or normally-derived offspring to the stress of cardiac puncture or of noise and shaking, while pituitary-adrenal responses to exposure to a novel environment, cold or 2-3 days of fasting were normal. Adrenal sensitivity to ACTH in dexamethasone-suppressed adult offspring was unaffected by the prenatal treatment. The results demonstrate that fetal ethanol exposure enhances adult pituitary-adrenal responses to certain stressors, including alcohol as demonstrated previously, and suggest that the long-term effects may be mediated by developmental actions of alcohol on central neural mechanisms involved in the regulation of this neuroendocrine system.
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PMID:Long-term effects of fetal ethanol exposure on pituitary-adrenal response to stress. 707 Oct 91


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