Levin E R, Sharp B, Weber M A, Drayer J I
Horm Res. 1986;23(4):193-9. doi: 10.1159/000180323.
The involvement of endogenous opioid peptides in the antihypertensive action of acutely administered clonidine, a centrally acting adrenergic agonist, was studied in humans. Eight hypertensive subjects received clonidine 0.2 mg orally, naloxone 8 mg i.v. followed by a 0.13 mg/min infusion, and both drugs together on separate days. Clonidine resulted in a significant decrease in mean blood pressure, which was not affected by concomitant treatment with naloxone. Naloxone alone or with clonidine caused significant elevations in plasma aldosterone, not mediated by increased plasma renin activity. Plasma beta-endorphin was not increased after clonidine administration. In humans, the antihypertensive effects of acute clonidine administration do not appear to be mediated by the release or action of endogenous opioids.
研究了内源性阿片肽在急性给予可乐定（一种中枢作用的肾上腺素能激动剂）的降压作用中的参与情况，研究对象为人类。八名高血压患者分别在不同日期口服0.2毫克可乐定、静脉注射8毫克纳洛酮，随后以0.13毫克/分钟的速度输注，以及同时给予这两种药物。可乐定导致平均血压显著下降，而纳洛酮的联合治疗对此无影响。单独使用纳洛酮或与可乐定联合使用会导致血浆醛固酮显著升高，这并非由血浆肾素活性增加介导。给予可乐定后血浆β-内啡肽未升高。在人类中，急性给予可乐定的降压作用似乎不是由内源性阿片类物质的释放或作用介导的。
