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(Hypertension. 2004;43:722.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

How Does Angiotensin II Cause Renal Injury?

From the Section of Nephrology, Hypertension, and Transplantation (D.L., K.L.P., R.J.J), University of Florida, Gainesville; and Department of Nephrology (J.H.-A.), Instituto Nacional de Cardiologia I. Chavez, Mexico City, Mexico.

Correspondence to Richard J. Johnson, Division of Nephrology, Hypertension, and Transplantation, University of Florida, P.O. Box 100224, Gainesville, FL 32610-224. E-mail johnsrj@medicine.ufl.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Based on several important clinical trials, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure 7 (JNC 7) approves the use of angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin receptor blockers (ARBs) in the first-line treatment for hypertension in subjects with chronic renal insufficiency, in diabetic subjects with proteinuria, and in black subjects with renal insufficiency and proteinuria, because these agents appear to provide renoprotection in these conditions.¹ The observation that agents that interfere with the renin-angiotensin system (RAS) might be useful in subjects with renal insufficiency seems at first to be counterintuitive, because many subjects with chronic renal insufficiency are volume-expanded, which acts to inhibit the RAS. However, in renal insufficiency, other mechanisms that stimulate renin may be involved, including intrarenal microvascular disease causing ischemia, hyperuricemia, and low 1,25-dihydroxyvitamin D levels. Renal injury will also activate renal afferent nerves to stimulate ß-adrenergic output from the central nervous system that can stimulate renin release. Activation of the local RAS has also been shown in renal injury, indicated by upregulation of ACE and the infiltration of leukocytes expressing angiotensin II.²

A variety of mechanisms has been suggested by which angiotensin II causes renal injury. Angiotensin II may cause pressure-induced renal injury via its ability to induce systemic and glomerular hypertension or cause ischemia-induced renal injury secondary to intrarenal vasoconstriction and decreased renal blood flow. Angiotensin may also cause tubular injury secondary to angiotensin-induced proteinuria. Angiotensin II also activates renal fibroblasts to become myofibroblasts, . . . [Full Text of this Article]

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