Gao Y
Zhonghua Yi Xue Za Zhi. 1990 Jun;70(6):327-9, 24.
To further study the relationship between endogenous opioid peptides and essential hypertension, we measured the concentrations of plasma leucine-enkephalin (LEK) and beta-endorphin (beta-EP) in 50 patients with essential hypertension by radioimmunoassay and investigated the effects of captopril on them. It was shown that the concentrations of plasma LEK and beta-EP in patients with essential hypertension were lower than those in normotensive subjects. No effects of age and sex were found on the concentrations of plasma LEK and beta-EP, and there was no difference in plasma LEK and beta-EP levels between patients with Stage I essential hypertension and those with Stage II essential hypertension. After a single dose of captopril, blood pressure and plasma angiotensin II decreased, plasma renin activity increased; and plasma LEK and beta-EP levels increased. Plasma LEK and beta-EP levels in patients with essential hypertension increased after one month of captopril treatment. In conclusion, the lower plasma LEK and beta-EP levels in patients with essential hypertension indicate that LEK and beta-EP may play a role in the pathogenesis of essential hypertension, and the depressor effects of captopril may act through LEK and beta-EP, besides blocking formation of angiotension II.
为进一步研究内源性阿片肽与原发性高血压之间的关系，我们采用放射免疫分析法测定了50例原发性高血压患者血浆亮氨酸脑啡肽（LEK）和β-内啡肽（β-EP）的浓度，并研究了卡托普利对其的影响。结果显示，原发性高血压患者血浆LEK和β-EP的浓度低于血压正常者。未发现年龄和性别对血浆LEK和β-EP浓度有影响，Ⅰ期原发性高血压患者与Ⅱ期原发性高血压患者的血浆LEK和β-EP水平也无差异。单次服用卡托普利后，血压和血浆血管紧张素Ⅱ降低，血浆肾素活性升高；血浆LEK和β-EP水平升高。卡托普利治疗1个月后，原发性高血压患者血浆LEK和β-EP水平升高。综上所述，原发性高血压患者血浆LEK和β-EP水平较低表明LEK和β-EP可能在原发性高血压的发病机制中起作用，卡托普利的降压作用除了阻断血管紧张素Ⅱ的形成外，可能还通过LEK和β-EP起作用。
