Bramnert M, Hökfelt B
J Clin Endocrinol Metab. 1984 Feb;58(2):374-7. doi: 10.1210/jcem-58-2-374.
Studies in animals and man indicate a functional interaction between the adrenergic and the opiate systems. In the present study the effect of the opiate receptor blocker naloxone on the increase in plasma GH induced by clonidine was investigated in eight patients with essential hypertension. In a randomized order the patients received a bolus dose of naloxone (10 micrograms/kg) or physiological saline followed by a slow infusion of naloxone (5 micrograms/kg X h) or saline, respectively. Fifteen minutes after the bolus dose of saline or naloxone, clonidine (3 micrograms/kg) was infused for 10 min. Clonidine induced a significant increase in plasma GH. Naloxone pretreatment resulted in a significantly reduced GH increase after the clonidine infusion. These results indicate that the clonidine-induced increase in plasma GH in hypertensive man is partly mediated via activation of opiate receptors which can be blocked by naloxone.
对动物和人类的研究表明,肾上腺素能系统和阿片系统之间存在功能相互作用。在本研究中,对8名原发性高血压患者研究了阿片受体阻滞剂纳洛酮对可乐定诱导的血浆生长激素(GH)升高的影响。患者按随机顺序接受一次大剂量纳洛酮(10微克/千克)或生理盐水,随后分别缓慢输注纳洛酮(5微克/千克×小时)或生理盐水。在给予生理盐水或纳洛酮大剂量15分钟后,输注可乐定(3微克/千克)10分钟。可乐定引起血浆GH显著升高。纳洛酮预处理导致可乐定输注后GH升高显著降低。这些结果表明,高血压患者中可乐定诱导的血浆GH升高部分是通过阿片受体激活介导的,而纳洛酮可阻断该受体。