Renal hemodynamics in essential and renovascular hypertension. Influence of captopril.
Among vascular beds, that of the kidney is especially responsive to angiotensin II, perhaps a reflection of the fact that the renin-angiotensin axis is normally a volume-control rather than a pressure-control system. The dose of angiotensin required to induce renal vasoconstriction in a normal subject receiving a typical, liberal sodium intake, for example, is about an order of magnitude lower than that required to induce a pressor response. Indeed, 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. In patients with essential hypertension, in whom renal vascular tone is commonly increased, converting enzyme inhibitors such as teprotide and captopril induce a potentiated acute renal vascular response: renal blood flow increases more than it does in normal subjects. The result is a consistent, early increase in sodium excretion and an occasional increase in glomerular filtration rate. Reduced aldosterone release consequent to 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 very well maintained. In renal artery stenosis the situation is more complex: as perfusion pressure distal to the stenosis falls, typically afferent arteriolar dilatation exists and glomerular capillary pressure tends to be maintained by an increase in postglomerular resistance. To the extent that this increase is angiotensin-mediated, suppression of angiotensin formation with captopril 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 when the stenosis is bilateral or involves a solitary kidney. The available evidence suggests that the converting enzyme inhibitor's influence on the kidney primarily reflects reduced angiotensin II formation, although reduced kinin degradation or increased prostaglandin synthesis may also have an influence. Whatever the mechanism responsible for the renal response, there are compelling reasons for suspecting that the salutary action of captopril on the kidney makes a substantial contribution to its over-all efficacy in the treatment of hypertension.
D058186:Acute Kidney Injury / Q000139:chemically induced; D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril / Q000009:adverse effects / Q000627:therapeutic use*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D006978:Hypertension, Renovascular / Q000188:drug therapy* / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects; D009318:Natriuresis / Q000187:drug effects; D011392:Proline / Q000031:analogs & derivatives*; D012077:Renal Artery / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects; D012964:Sodium / Q000378:metabolism; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D011392:Proline; D002216:Captopril; D012964:Sodium