MacGregor G A, Markandu N D, Banks R A, Bayliss J, Roulston J E, Jones J C
Br Med J (Clin Res Ed). 1982 Mar 6;284(6317):693-6. doi: 10.1136/bmj.284.6317.693.
Twenty-four patients with moderate to severe hypertension were treated for four weeks with captopril, an oral inhibitor of angiotensin-converting enzyme. The fall in blood pressure with captopril alone correlated with pretreatment plasma renin activity. The effect of adding either hydrochlorothiazide or propranolol to the captopril treatment was then studied. The addition of hydrochlorothiazide to captopril produced a dose-dependent fall in blood pressure. At the higher dose of the diuretic this fall in blood pressure correlated with weight loss, suggesting that when the diuretic-induced compensatory rise in angiotensin II is prevented by captopril the fall in blood pressure becomes dependent on loss of sodium and water. In contrast, the addition of propranolol to captopril produced no further fall in blood pressure, suggesting that inhibition of angiotensin-converting enzyme prevents the blood pressure lowering effect of propranolol. This may have implications for the mechanism whereby beta-blockers alone lower blood pressure. These contrasting effects of hydrochlorothiazide and propranolol in the presence of captopril indicate that in patients whose hypertension is not controlled by captopril alone the addition of increasing doses of diuretic is likely to control the blood pressure. The addition of a beta-blocker, however, is less likely to be effective.
24例中重度高血压患者接受了口服血管紧张素转换酶抑制剂卡托普利治疗四周。单独使用卡托普利时血压下降与治疗前血浆肾素活性相关。随后研究了在卡托普利治疗基础上加用氢氯噻嗪或普萘洛尔的效果。卡托普利加用氢氯噻嗪可使血压呈剂量依赖性下降。在利尿剂较高剂量时,这种血压下降与体重减轻相关,提示当卡托普利阻止利尿剂引起的血管紧张素II代偿性升高时,血压下降依赖于钠和水的丢失。相反,卡托普利加用普萘洛尔未使血压进一步下降,提示血管紧张素转换酶抑制可阻止普萘洛尔的降压作用。这可能对β受体阻滞剂单独降压的机制有影响。氢氯噻嗪和普萘洛尔在卡托普利存在时的这些不同作用表明,对于单独使用卡托普利不能控制高血压的患者,增加利尿剂剂量可能控制血压。然而,加用β受体阻滞剂不太可能有效。