Morioka S, Simon G, Cohn J N
Clin Pharmacol Ther. 1983 Nov;34(5):583-9. doi: 10.1038/clpt.1983.219.
Systolic time measurements, echocardiography, and bicycle exercise testing with cardiac output determinations (CO2 rebreathing) were used to evaluate cardiac performance in 16 male hypertensives at the end of a 4-wk placebo period and after 12 wk of treatment with increasing doses (maximum = 40 mg/day) of enalapril maleate (N = 11) and of placebo (N = 5). The effect of exercise on plasma renin activity (PRA) and plasma norepinephrine (NE) concentration was also measured. Mean arterial pressure was reduced by 10 mm Hg or more in all but one subject who received enalapril. In both the enalapril- and placebo-treated subjects, the preejection period/left ventricular ejection time ratio and fractional shortening of the left ventricle at rest and cardiac output and stroke volume during moderate exercise did not change during the study. Enalapril induced a compensatory rise in PRA (N = 10). Compared to plasma NE concentration, 1124 +/- 380 pg/ml (mean +/- SD), during exercise at the end of the initial placebo period, there was attenuation of the rise of plasma NE concentration, 851 +/- 290, at the same load of exercise during enalapril therapy. Unchanged cardiac performance despite effective long-term lowering of blood pressure with enalapril may relate to inhibition of angiotensin II-mediated facilitation of NE release from peripheral nerve endings.
在为期4周的安慰剂期结束时以及用马来酸依那普利（最大剂量=40毫克/天）递增剂量治疗12周后（N=11）和安慰剂治疗后（N=5），对16名男性高血压患者进行收缩期时间测量、超声心动图检查以及测定心输出量（二氧化碳重呼吸法）的自行车运动试验，以评估心脏功能。还测量了运动对血浆肾素活性（PRA）和血浆去甲肾上腺素（NE）浓度的影响。除一名接受依那普利治疗的受试者外，所有受试者的平均动脉压均降低了10毫米汞柱或更多。在接受依那普利和安慰剂治疗的受试者中，研究期间静息时的射血前期/左心室射血时间比值、左心室缩短分数以及中等强度运动时的心输出量和每搏输出量均未改变。依那普利使PRA代偿性升高（N=10）。与初始安慰剂期结束时运动期间的血浆NE浓度1124±380皮克/毫升（平均值±标准差）相比，依那普利治疗期间相同运动负荷下血浆NE浓度升高幅度减弱，为851±290。尽管依那普利能有效长期降低血压，但心脏功能未改变，这可能与抑制血管紧张素II介导的外周神经末梢NE释放促进作用有关。
