Suemaru S, Dallman M F, Darlington D N, Cascio C S, Shinsako J
Department of Physiology, School of Medicine, University of California, San Francisco.
Neuroendocrinology. 1989 Feb;49(2):181-90. doi: 10.1159/000125112.
The role of alpha-adrenergic mechanism in the acute effects of morphine in the hypothalamo-pituitary-adrenocortical (HPA) and cardiovascular (CV) systems, and the interrelationship between the HPA and CV responses to alpha-adrenoceptor antagonists and/or morphine were studied by peripheral administration of prazosin, a selective alpha 1-adrenoceptor antagonist, and yohimbine, a selective alpha 2-adrenoceptor antagonist, in conscious, unstressed or ether-stressed rats. The test substances were administered intravenously or intraperitoneally in chronically cannulated or noncannulated rats. In the i.v. experiment, morphine (1 mg/100 g BW) rapidly induced a pronounced bradycardia and a short-lasting fall in blood pressure (BP), followed by a rise in BP, and increased plasma corticosterone concentration. Prazosin (0.5 mg/kg BW) induced a rapid fall in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with prazosin did not block the effect of morphine on the CV system, but abolished the morphine-induced increment in plasma corticosterone concentration. Yohimbine (0.5 mg/kg BW) induced a rapid and a subsequent slowly developing rise in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with yohimbine did not block the effect of morphine on the CV system nor alter the stimulatory effect of morphine on the secretion of corticosterone. In the intraperitoneal experiment, morphine (2 mg/100 g BW) stimulated the secretion of adrenocorticotropic hormone (ACTH) and corticosterone and prazosin (1 mg/kg BW) stimulated the secretion of corticosterone, but pretreatment with prazosin reduced the morphine-induced increment in plasma corticosterone concentration in unstressed rats. In stressed rats, morphine reduced the stress-induced increment in plasma ACTH and corticosterone concentrations and prazosin also reduced the stress-induced increment in plasma corticosterone concentration. Pretreatment with prazosin did not alter the inhibitory effect of morphine...
通过对清醒、未应激或乙醚应激的大鼠外周给予选择性α1-肾上腺素能受体拮抗剂哌唑嗪和选择性α2-肾上腺素能受体拮抗剂育亨宾，研究了α-肾上腺素能机制在吗啡对下丘脑-垂体-肾上腺皮质（HPA）和心血管（CV）系统急性作用中的作用，以及HPA和CV对α-肾上腺素能受体拮抗剂和/或吗啡反应之间的相互关系。受试物质通过静脉注射或腹腔注射给予慢性插管或未插管的大鼠。在静脉注射实验中，吗啡（1mg/100g体重）迅速引起明显的心动过缓和短暂的血压下降，随后血压升高，并增加血浆皮质酮浓度。哌唑嗪（0.5mg/kg体重）引起血压迅速下降和心动过速，并增加血浆皮质酮浓度。哌唑嗪预处理并未阻断吗啡对心血管系统的作用，但消除了吗啡诱导的血浆皮质酮浓度升高。育亨宾（0.5mg/kg体重）引起血压迅速升高，随后缓慢升高，以及心动过速，并增加血浆皮质酮浓度。育亨宾预处理并未阻断吗啡对心血管系统的作用，也未改变吗啡对皮质酮分泌的刺激作用。在腹腔注射实验中，吗啡（2mg/100g体重）刺激促肾上腺皮质激素（ACTH）和皮质酮的分泌，哌唑嗪（1mg/kg体重）刺激皮质酮的分泌，但哌唑嗪预处理降低了未应激大鼠中吗啡诱导的血浆皮质酮浓度升高。在应激大鼠中，吗啡降低了应激诱导的血浆ACTH和皮质酮浓度升高，哌唑嗪也降低了应激诱导的血浆皮质酮浓度升高。哌唑嗪预处理并未改变吗啡的抑制作用……
