Zolotov N A, Kiriaev A A, Merzon A K, Mukharliamov N M
Ter Arkh. 1988;60(8):46-51.
The effect of captopril on renal function, central hemodynamics and the hormonal status was studied in 14 patients with chronic congestive heart failure in single administration of the drug at a dose of 25 mg and during short-term course therapy at a daily dose of 75 mg for 7 days. Captopril single administration was shown to cause an increase in natriuresis by 121% and diuresis by 120%. Correlation analysis showed that the natriuretic effect of captopril resulted from a decrease in tubular sodium reabsorption which, in its turn, was determined by a decrease in the production of angiotensin II and changes of pritubular circulation. Seven-day course therapy was accompanied by the patients' improved general status, improved indices of hemodynamics, and better tolerance to physical exercise. At the same time diuresis and renal excretion of sodium were above the basal level by 113 and 86%, respectively. It can be assumed that this natriuretic effect was determined by the suppression of angiotensin II, aldosterone and probably norepinephrine and vasopressin production. The analysis has shown that a favorable captopril renal effect is not mediated through improved central hemodynamics but results from changes of the hormonal and neurohumoral status.
对14例慢性充血性心力衰竭患者进行研究,观察卡托普利单次给予25mg剂量以及短期疗程治疗(每日剂量75mg,共7天)时对肾功能、中心血流动力学和激素状态的影响。结果显示,卡托普利单次给药可使尿钠排泄增加121%,尿量增加120%。相关性分析表明,卡托普利的利钠作用源于肾小管钠重吸收减少,而这又取决于血管紧张素II生成减少和肾小管周围循环的改变。为期7天的疗程治疗使患者的一般状况得到改善,血流动力学指标好转,对体育锻炼的耐受性增强。同时,尿量和尿钠排泄分别比基础水平高出113%和86%。可以推测,这种利钠作用是由血管紧张素II、醛固酮以及可能还有去甲肾上腺素和血管升压素生成受到抑制所决定的。分析表明,卡托普利对肾脏的有益作用并非通过改善中心血流动力学介导,而是由激素和神经体液状态的改变所致。