Farber M O, Weinberger M H, Robertson G L, Fineberg N S
Department of Medicine, Indiana University School of Medicine, Indianapolis.
Am Rev Respir Dis. 1987 Oct;136(4):862-6. doi: 10.1164/ajrccm/136.4.862.
Ten clinically stable, hypercapneic patients with advanced chronic obstructive pulmonary disease were studied to assess the effect of angiotensin-converting enzyme blockade on their inability to excrete a sodium load. Renal, hormonal, and cardiovascular responses to sodium loading were determined during two 5.5-h studies: control day, placebo; and experimental day, captopril. At baseline, compared with control subjects, patients displayed a decrease in urinary sodium associated with low effective renal plasma flow and high plasma level of aldosterone. Captopril, given before sodium loading, produced a significant increase in urinary sodium without increasing effective renal plasma flow and without suppressing plasma aldosterone more than sodium loading alone. Thus, the mechanism by which angiotensin-converting enzyme inhibition induces an acute sodium diuresis in these patients remains to be elucidated. The blockade of angiotensin with captopril also affected the osmotic regulation of vasopressin: for a given increase in plasma osmolality, the increase in plasma vasopressin was subnormal, a finding consistent with the hypothesis that angiotensin II contributes to the regulation of vasopressin secretion.
对10名临床状况稳定、存在高碳酸血症的晚期慢性阻塞性肺疾病患者进行了研究，以评估血管紧张素转换酶阻断对其排钠能力下降的影响。在两项时长均为5.5小时的研究中，测定了钠负荷情况下的肾脏、激素及心血管反应：对照日，给予安慰剂；实验日，给予卡托普利。在基线状态下，与对照受试者相比，患者尿钠减少，同时有效肾血浆流量降低，血浆醛固酮水平升高。在钠负荷前给予卡托普利，可使尿钠显著增加，而有效肾血浆流量未增加，且血浆醛固酮的抑制程度未超过单纯钠负荷时。因此，血管紧张素转换酶抑制在这些患者中诱导急性利钠的机制仍有待阐明。用卡托普利阻断血管紧张素也影响了血管升压素的渗透调节：在血浆渗透压给定的升高幅度下，血浆血管升压素的升高低于正常水平，这一发现与血管紧张素II参与血管升压素分泌调节的假说一致。
