Giudicelli J F, Berdeaux A, Edouard A, Richer C, Jacolot D
Br J Clin Pharmacol. 1985 Sep;20(3):211-8. doi: 10.1111/j.1365-2125.1985.tb05063.x.
The effects of enalapril, 20 mg orally, on the responses to baroreflex activation and deactivation by respectively phenylephrine and nitroglycerin were investigated in normotensive subjects on a normal sodium diet, with simultaneous measurement of plasma renin activity (PRA), converting enzyme activity (PCEA), aldosterone and catecholamines. Enalapril, 4 h after administration, lowered artificial blood pressure without modifying heart rate and plasma catecholamines. PCEA was abolished, PRA increased and plasma aldosterone decreased. Enalapril (a) displaced to the left the baroreflex set-point, (b) did not affect baroreflex sensitivity since the slopes of the RR-interval/systolic blood pressure regression lines remained unchanged during both activation and deactivation and (c) did not modify baroreflex efficacy since the maximal RR-interval responses as well as the overall RR-interval-time products to identical blood pressure variations were not modified. Thus, enalapril induced a resetting of the baroreflex, which probably accounts for the lack of reflex tachycardia observed during the drug-induced fall in blood pressure.
在正常钠饮食的血压正常受试者中,研究了口服20毫克依那普利对分别由去氧肾上腺素和硝酸甘油引起的压力反射激活和失活反应的影响,同时测量血浆肾素活性(PRA)、转化酶活性(PCEA)、醛固酮和儿茶酚胺。给药4小时后,依那普利降低了人为血压,但未改变心率和血浆儿茶酚胺。PCEA被消除,PRA升高,血浆醛固酮降低。依那普利(a)使压力反射调定点向左移位,(b)不影响压力反射敏感性,因为在激活和失活过程中RR间期/收缩压回归线的斜率保持不变,并且(c)不改变压力反射效能,因为对相同血压变化的最大RR间期反应以及总体RR间期时间乘积未被改变。因此,依那普利引起了压力反射的重新设定,这可能解释了在药物诱导的血压下降期间未观察到反射性心动过速的原因。