Christlieb A R
Diabetes. 1976;25(2 SUPPL):820-5.
The renin-angiotensin-aldosterone system appears to function normally in uncomplicated diabetes mellitus. Alterations in this system, however, have been observed in several of the microvascular and electrolyte complications associated with this disease. Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism. PRA is low in rats with uncontrolled, nonketotic diabetes, and pressor responsiveness to angiotension II is increased in patients with diabetic retinopathy. Potential mechanisms responsible for the decreased PRA include plasma volume expansion, hyalin destruction of the juxtaglomerular cells, defective synthesis of renin, and inadequate catecholamine stimulation of renin, and inadequant cathecholamine stimulation of renin release. In diabetic ketoacidosis, PRA and aldosterone are stimulated secondary to the associated dehydration with hypovolemia. This report reviews the current status of the function of the renin-angiotensin-aldosterone system in diabetes mellitus and proposes a possible role for the altered function of this system in the pathophysiology of several diabetic complications.
肾素-血管紧张素-醛固酮系统在无并发症的糖尿病中似乎功能正常。然而，在与该疾病相关的一些微血管和电解质并发症中已观察到该系统的改变。在患有肾病和高血压的糖尿病患者、患有包括体位性低血压在内的神经病变的患者以及患有醛固酮减少症的患者中，血浆肾素活性（PRA）和醛固酮降低。在未控制的非酮症糖尿病大鼠中PRA较低，而在糖尿病视网膜病变患者中对血管紧张素II的升压反应性增加。导致PRA降低的潜在机制包括血容量扩张、肾小球旁细胞的玻璃样破坏、肾素合成缺陷、儿茶酚胺对肾素的刺激不足以及儿茶酚胺对肾素释放的刺激不足。在糖尿病酮症酸中毒中，PRA和醛固酮因伴有血容量不足的脱水而继发性升高。本报告综述了糖尿病中肾素-血管紧张素-醛固酮系统功能的现状，并提出该系统功能改变在几种糖尿病并发症病理生理学中的可能作用。
