Angiotensin-converting enzyme inhibition: renal aspect.
Angiotensin-converting enzyme inhibition: renal aspect.
复制标题
血管紧张素转换酶抑制：肾脏方面。
DOI：
10.1097/00005344-198507001-00009
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发表时间：
1985
影响因子：
3
通讯作者：
Hollenberg,NK
中科院分区：
文献类型：
--
作者：
Hollenberg,NK
Compelling arguments can be made for a local, intrarenal role as angiotensin's first action in phylogeny, with additional cardiovascular and endocrine responses arising later. Perhaps for that reason the vascular bed of the kidney is especially responsive to angiotensin II. Conversely, when the renin-angiotensin system is activated, as it is when sodium intake is restricted or diuretics are administered, the renal blood supply shows the most striking and consistent vasodilatation among vascular beds assessed after converting enzyme inhibition. When renal vascular tone is increased in patients with essential hypertension, converting enzyme inhibitors induce a potentiated acute renal vascular response: renal blood flow increases more than it does in normal subjects, with an associated consistent early increase in sodium excretion and an occasional increase in glomerular filtration rate. Reduced aldosterone release consequent on the block of angiotensin II formation also contributes to the natriuresis and results in positive potassium balance. With long-term therapy renal function tends to be well maintained. The response to converting enzyme inhibition in renal artery stenosis is more complex: as perfusion pressure distal to the stenosis falls there is typical afferent arteriolar dilatation and glomerular capillary pressure tends to be maintained by a rise in postglomerular resistance. To the extent that this is angiotensin mediated, suppression of angiotensin formation can reduce glomerular capillary pressure and thus filtration rate. This is well tolerated in the patient with unilateral stenosis and a healthy contralateral kidney, but can provoke renal failure where the stenosis is bilateral or involves a solitary kidney. The evidence suggests that the converting enzyme inhibitors' influence on the kidney primarily reflects reduced angiotensin II formation, although an influence by way of reduced kinin degradation or increased prostaglandin synthesis is also possible. Whatever the mechanism responsible for the renal response, there are compelling reasons for suspecting that the salutary action of ACE inhibition on the kidney makes a substantial contribution to its overall efficacy in the treatment of hypertension.
