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热应激后温度调节和抗利尿激素调节中心的环磷酸腺苷

cAMP in temperature- and ADH-regulating centers after thermal stress.

作者信息

Kornbluth I, Siegel R A, Conforti N, Chowers I

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1977 Feb;42(2):257-61. doi: 10.1152/jappl.1977.42.2.257.

Abstract

cAMP concentrations in temperature-regulating sites of the brain and plasma osmolality were measured after exposure of male rats to 36 degrees C and 37-42% rh. for 10, 20, or 30 min. Plasma osmolality was affected by none of the heat exposures. In both the preoptic area and the posterior medial hypothalamus, cAMP concentrations were increased compared to controls, after 10, 20 and 30 min of heat exposure. In the supraoptic-paraventricular nuclei, neither 10 nor 20 min of exposure resulted in augmented cAMP concentrations; but after 30 min of heat exposure, cAMP levels in these nuclei were significantly greater than in controls. Neurohypophysial cAMP concentrations were increased after both 10 and 30 min of exposure. Cerebral cortical cAMP concentrations were not affected by thermal stress. It is concluded that cAMP is involved in the neural mechanisms which are brought into play to regulate body temperature during acute heat exposure. The significance of this involvement and its relation to the overall temperature-regulating mechanisms of the body are discussed.

摘要

将雄性大鼠暴露于36摄氏度、相对湿度37 - 42%的环境中10、20或30分钟后,测量其大脑体温调节部位的环磷酸腺苷(cAMP)浓度和血浆渗透压。所有热暴露均未影响血浆渗透压。在视前区和下丘脑后内侧,热暴露10、20和30分钟后,与对照组相比,cAMP浓度升高。在视上核 - 室旁核中,10分钟和20分钟的暴露均未导致cAMP浓度升高;但热暴露30分钟后,这些核中的cAMP水平显著高于对照组。神经垂体的cAMP浓度在暴露10分钟和30分钟后均升高。大脑皮层的cAMP浓度不受热应激影响。得出的结论是,cAMP参与了急性热暴露期间调节体温的神经机制。讨论了这种参与的意义及其与身体整体体温调节机制的关系。

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