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(Hypertension. 2003;41:193.)
© 2003 American Heart Association, Inc.

Editorial Commentary

False Claims of Blood Pressure–Independent Protection by Blockade of the Renin Angiotensin Aldosterone System?

From the Department of Laboratory Medicine, University of California, San Francisco, Calif.

Correspondence to Theodore W. Kurtz, MD, Professor of Laboratory Medicine, 505 Parnassus Avenue, Room L518, UCSF Medical Center, Box 0134, San Francisco, CA 94143-0134. E-mail KurtzT@Labmed2.ucsf.edu

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

	Introduction

 
In the wake of a number of recent clinical trials, claims that blockade of the renin-angiotensin-aldosterone system (RAAS) provides vascular protective effects that are not simply secondary to reductions in blood pressure (so-called BP-independent effects) have become increasingly popular. How accurate are these kinds of claims? The report by Griffin, Bidani, and coworkers in this issue of Hypertension¹ is one of a series of studies from this group in animal models of hypertension that, together with recent clinical studies by other investigators, have begun to raise serious questions about such claims regarding RAAS blockade.

In the current study of RAAS blockade in the stroke-prone spontaneously hypertensive rat (SHRsp) and in previous studies in the remnant kidney model of hypertension, Griffin et al have done something that should be axiomatic for those involved in blood pressure research yet is ironically neglected in many, if not most, clinical and experimental studies of hypertension: they have paid careful attention to obtaining an accurate and thorough assessment of the blood pressure profile. By using radiotelemetry to obtain continuous, 24-hour measurements of blood pressure throughout the course of their studies, Griffin et al have demonstrated that the renoprotection afforded by enalapril or spironolactone in salt-supplemented SHRsp is tightly related to the effects of these agents on blood pressure. These results are similar to their earlier radiotelemetry studies of ACE inhibition or angiotensin receptor blockade in the remnant kidney model of hypertension showing a highly robust relationship between blood pressure and renoprotection that is remarkable when . . . [Full Text of this Article]

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