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(Hypertension. 2008;51:811.)
© 2008 American Heart Association, Inc.

Brief Review

Kidney in Hypertension

Guyton Redux

From the Division of Nephrology, Department of Medicine, Duke University and Durham Veterans’Affairs Medical Centers, Durham, NC.

Correspondence to Thomas M. Coffman, Room 2018 MSRB2, 106 Research Dr, Duke University Medical Center, Durham, NC 27710. E-mail tcoffman@duke.edu

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

	Introduction

 
Regulation of blood pressure is a complex integrated response involving a variety of organ systems including the central nervous system (CNS), cardiovascular system, kidneys, and adrenal glands. These systems modulate cardiac output, fluid volumes, and peripheral vascular resistance, the key determinants of blood pressure. More than 40 years ago, Guyton and Coleman¹ developed computer models of arterial pressure control, attempting to incorporate the known variables impacting blood pressure homeostasis. The conclusion of this analysis was that regulation of sodium excretion by the kidney and consequent effects on body fluid volumes made up the critical pathway determining the chronic level of intra-arterial pressure.

	The Renin-Angiotensin System and Blood Pressure Control

 
Our own studies of the physiology of blood pressure regulation have focused on the renin-angiotensin (Ang) system (RAS) using genetically modified mouse models. Highly conserved through phylogeny, the RAS is an essential regulator of blood pressure and fluid balance. This biological system is a multienzymatic cascade in which angiotensinogen, its major substrate, is processed in a 2-step reaction by renin and Ang-converting enzyme (ACE), resulting in the sequential generation of Ang I and Ang II. Along with its importance in maintaining normal circulatory homeostasis, abnormal activation of the RAS can contribute to the development of hypertension and target organ damage. The importance of the RAS in clinical medicine is highlighted by the impressive efficacy of pharmacological agents that inhibit the synthesis or activity of Ang II.^2–5

At the cellular level, responsiveness to Ang II is conferred by expression of Ang receptors. Ang receptors can be divided into 2 . . . [Full Text of this Article]

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