Coppola L, Cozzolino D, Giugliano D, Verrazzo G, Tirelli A, Giunta R, Buoninconti R, Torella R
Department of Geriatrics and Metabolic Diseases, Second University of Naples, Italy.
J Clin Endocrinol Metab. 1994 Sep;79(3):826-30. doi: 10.1210/jcem.79.3.8077368.
The purpose of the present study was to determine if opioid agonism (beta-endorphin) and antagonism (Naloxone) exert rheological and cardiovascular effects in normal humans and in patients with essential hypertension. Eight hypertensive patients were matched for age, sex, and body habitus (body mass index, waist to hip ratio) with eight normotensive healthy subjects. In all subjects, heart rate and blood pressure (continuous automatic recording), blood and plasma viscosity, fibrinogen, hematocrit, and platelet aggregation to ADP were evaluated during an infusion of human synthetic beta-endorphin (0.5 mg/h). On a different day and in randomized order, the subjects were submitted to another beta-endorphin infusion preceded by an i.v. naloxone bolus (5 mg in 5 min). beta-Endorphin and naloxone failed to significantly alter heart rate or blood pressure in both normotensive and hypertensive subjects. In hypertensive patients, beta-endorphin significantly increased blood viscosity and ADP-induced platelet aggregation, but only the former effect was naloxone-sensitive. In normotensive subjects, beta-endorphin caused a transient but significant decrease of platelet aggregation that was reversed by naloxone. These data suggest that beta-endorphin may play some role in the inhibitory control of platelet aggregation in normal subjects. An altered responsiveness of some rheological determinants to beta-endorphin seems to be present in human hypertension.
本研究的目的是确定阿片类激动剂（β-内啡肽）和拮抗剂（纳洛酮）对正常人和原发性高血压患者是否产生流变学和心血管效应。8名高血压患者与8名血压正常的健康受试者在年龄、性别和身体状况（体重指数、腰臀比）方面进行了匹配。在所有受试者中，在输注人工合成β-内啡肽（0.5mg/h）期间评估心率和血压（连续自动记录）、血液和血浆粘度、纤维蛋白原、血细胞比容以及血小板对ADP的聚集情况。在另一天，受试者按随机顺序先静脉注射一剂纳洛酮（5mg，5分钟内注射完毕），然后再输注β-内啡肽。β-内啡肽和纳洛酮均未使血压正常和高血压受试者的心率或血压发生显著改变。在高血压患者中，β-内啡肽显著增加血液粘度和ADP诱导的血小板聚集，但只有前者的效应可被纳洛酮逆转。在血压正常的受试者中，β-内啡肽使血小板聚集出现短暂但显著的降低，且这种降低可被纳洛酮逆转。这些数据表明，β-内啡肽可能在正常受试者血小板聚集的抑制性控制中发挥一定作用。在人类高血压中似乎存在一些流变学决定因素对β-内啡肽的反应性改变。
