Atkinson A B, Morton J J, Brown J J, Davies D L, Fraser R, Kelly P, Leckie B, Lever A F, Robertson J I
Br Heart J. 1980 Sep;44(3):290-6. doi: 10.1136/hrt.44.3.290.
The effect of the converting enzyme inhibitor captopril on arterial pressure, the components of the renin-angiotensin-aldosterone system, and body sodium and potassium content was studied in eight hypertensive patients with renal artery stenosis and, in conjunction with diuretics, in seven patients with hypertension unresponsive to previous treatment. Two hours after the first dose, captopril caused significant falls in systolic and diastolic pressures, plasma angiotensin II, and aldosterone, with converse increases in angiotensin I and both active and total renin; the initial fall in diastolic pressure was significantly related to the drop in plasma angiotensin II. The biochemical changes were sustained during prolonged treatment, even when diuretics were added. One untreated patient with renal artery occlusion had severe secondary aldosterone excess, was sodium and potassium depleted, and severely hyponatraemic and hypokalaemic; captopril restored blood pressure, plasma electrolyte concentrations, and exchangeable sodium and total body potassium to normal. In one man with renal artery stenosis and overall renal impairment captopril led to sodium retention, and blood pressure did not fall until a diuretic was added. In the remaining patients with renal artery stenosis, pretreatment renin, angio tensin II, and aldosterone concentrations were either normal or only modestly raised, and plasma electrolyte concentrations and body content of sodium and potassium were normal. Captopril alone controlled arterial pressure in all, three cases showing a gradual fall of pressure over the first six weeks of treatment; no significant changes in exchangeable sodium or total body potassium were seen. The group of patients with previously intractable hypertension were all controlled with a combination of captopril and diuretic.
研究了转换酶抑制剂卡托普利对8例肾动脉狭窄高血压患者动脉压、肾素 - 血管紧张素 - 醛固酮系统各组分以及机体钠和钾含量的影响,并在7例对先前治疗无反应的高血压患者中联合利尿剂进行了研究。首次给药后两小时,卡托普利使收缩压和舒张压、血浆血管紧张素II和醛固酮显著下降,而血管紧张素I以及活性肾素和总肾素则相反升高;舒张压的初始下降与血浆血管紧张素II的下降显著相关。即使添加利尿剂,在长期治疗期间生化变化仍持续存在。1例未经治疗的肾动脉闭塞患者存在严重的继发性醛固酮增多症,钠和钾耗竭,严重低钠血症和低钾血症;卡托普利使血压、血浆电解质浓度、可交换钠和全身钾恢复正常。在1例肾动脉狭窄且有整体肾功能损害的男性患者中,卡托普利导致钠潴留,直到添加利尿剂后血压才下降。在其余肾动脉狭窄患者中,治疗前肾素、血管紧张素II和醛固酮浓度正常或仅轻度升高,血浆电解质浓度以及钠和钾的机体含量正常。单独使用卡托普利可控制所有患者的动脉压,3例患者在治疗的前六周血压逐渐下降;可交换钠或全身钾未见明显变化。先前难治性高血压患者组均通过卡托普利和利尿剂联合治疗得到控制。