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(Hypertension. 2004;43:533.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

ACE Inhibition and Bradykinin-Mediated Renal Vascular Responses

EDHF Involvement

From Vascular Biology Center, Department of Physiology, Medical College of Georgia, Augusta.

Correspondence to Dr John D. Imig, Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500. E-mail jdimig@mail.mcg.edu

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

Angiotensin-converting enzyme (ACE) is known to catalyze the conversion of angiotensin I to angiotensin II and degrades bradykinin and other vasoactive peptides. The fact that ACE participates in the degradation of bradykinin has led to the postulate that the beneficial renal and cardiovascular actions of ACE inhibitors can be attributed to augmenting and prolonging the effects of bradykinin. These beneficial actions have been attributed to bradykinin stimulation of nitric oxide (NO) generation. The report by Matsuda et al in this issue of Hypertension¹ provides initial evidence that the renal hemodynamic change in response to ACE inhibition and elevated bradykinin levels is also mediated by an endothelium-derived hyperpolarizing factor (EDHF). In addition, this renal vascular action of ACE inhibition provides greater hemodynamic and natriuretic effects in the presence of angiotensin type 1 receptor blockers (ARBs). Does this finding suggest that ACE inhibitors have yet another additional renal and cardiovascular beneficial effect not associated with ARBs? Thus, the debate regarding the renal and cardiovascular benefits of ACE inhibitors, ARBs, or combined therapy now includes the possible involvement of EDHF.

ACE Inhibition, Bradykinin, and Renal Vascular EDHF

In the current study, canine afferent and efferent arteriolar diameter responses of superficial and juxtamedullary nephrons were evaluated in vivo by intravital CCD camera videomicroscopy. As was demonstrated by this group in an earlier study,² ARB treatment dilated afferent and efferent arterioles in the superficial and juxtamedullary regions. In the presence of the ARB, ACE inhibition resulted in a small dilation of the superficial efferent arteriole whereas it caused a much larger dilation . . . [Full Text of this Article]

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