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(Hypertension. 2005;45:477.)
© 2005 American Heart Association, Inc.

Hypertension Highlights

Endothelin, Angiotensin, and Oxidative Stress in Hypertension

From the Vascular Biology Center, Medical College of Georgia, Augusta.

Correspondence to David M. Pollock, PhD, Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500. E-mail dpollock@mcg.edu

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

	Introduction

 
Endothelin (ET)-1 is a potent vasoconstrictor and mitogen, and because of these properties, it is thought to play a role in the development of hypertension.^1,2 The vascular endothelium is a major source of ET-1 production, although a variety of other cell types also have been shown to synthesize and release ET-1. ET-1 is believed to act in a paracrine manner on ET_A and ET_B receptors on smooth muscle, which mediate contraction, cell proliferation, and hypertrophy. Activation of ET_B receptors on endothelial cells stimulates the production of prostacyclin and nitric oxide to induce vasorelaxation and inhibition of sodium transport in renal tubules. Given these properties, considerable attention has been paid to the mechanisms of ET-1 action as it relates to the renal control of blood pressure and the pathogenesis of salt-dependent hypertension. Renal ET synthesis is increased in experimental animals maintained on a high-salt diet and ET_A receptor antagonists lower arterial pressure primarily in salt-dependent models of hypertension.^1,2

For the past 30 to 40 years, the actions of angiotensin (Ang) II has been arguably the most widely investigated factor in hypertension research. Although physiology textbooks agree on the major actions of Ang II, eg, vasoconstriction and release of aldosterone, recent attention has focused on its ability to stimulate the synthesis of ET-1,^3–5 as well as reactive oxygen species.⁶ There are many reactive oxygen species such as superoxide, hydroxyl radical, and hydrogen peroxide that are produced by all cell types and can have profound effects on the vascular system to impact blood . . . [Full Text of this Article]

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