Rivier C, Vale W
Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, California 92037.
Alcohol Clin Exp Res. 1988 Apr;12(2):206-10. doi: 10.1111/j.1530-0277.1988.tb00181.x.
The intraperitoneal infusion of ethanol (EtoH) (1 g/hr/kg body weight for 3 hr) to intact rats blunted the secretion of adrenocorticotropic hormone (ACTH) and beta-endorphin induced by a subsequent 10-min exposure to mild, inescapable electroshocks (1.5 mA; 2 sec; four shocks/min) or by corticotropin-releasing factor (CRF). Conversely, administration of the shocks for 3 hr diminished the pituitary response to an acute i.p. injection of EtoH. While we have previously shown (Rivier C, Vale W: Endocrinology 121:1320-1328, 1987) that prolonged stress induces a loss of pituitary responsiveness due to the depletion of pituitary ACTH stores, the infusion of EtoH did not cause statistically significant changes in pituitary ACTH content. In adrenalectomized rats, the infusion of EtoH caused an elevation of ACTH plasma levels that was significantly (p less than or equal to 0.01) larger than intact animals. These rats also showed a blunted pituitary response to the acute injection of CRF, possibly because they were already secreting ACTH at a maximal rate. These results support the hypothesis that CRF, stress, and alcohol do not potentiate each other on pituitary ACTH and beta-endorphin secretion.
向完整无损的大鼠腹腔内输注乙醇(EtoH)(1克/小时/千克体重,持续3小时),可减弱随后10分钟暴露于轻度不可逃避电击(1.5毫安;2秒;每分钟4次电击)或促肾上腺皮质激素释放因子(CRF)所诱导的促肾上腺皮质激素(ACTH)和β-内啡肽的分泌。相反,给予电击3小时会减弱垂体对急性腹腔注射EtoH的反应。虽然我们之前已经表明(Rivier C,Vale W:《内分泌学》121:1320 - 1328,1987),长期应激会由于垂体ACTH储备的耗尽而导致垂体反应性丧失,但输注EtoH并未引起垂体ACTH含量的统计学显著变化。在肾上腺切除的大鼠中,输注EtoH导致ACTH血浆水平升高,且显著高于完整无损的动物(p小于或等于0.01)。这些大鼠对急性注射CRF的垂体反应也减弱,可能是因为它们已经以最大速率分泌ACTH。这些结果支持了以下假设:CRF、应激和酒精在垂体ACTH和β-内啡肽分泌方面不会相互增强。