Key result
A relative malfunction of the nitric oxide system and its imbalance with angiotensin II and endothelin-1 contribute to altered vascular tone, structural remodeling, and end-organ injury in hypertension.
This review highlights the complex interplay between nitric oxide, angiotensin II, and endothelin-1 in regulating vascular homeostasis and the pathophysiology of hypertension.
Hypothesis-generating for nitric oxide pathways in hypertension; should not yet change practice.
Nitric oxide, the metabolic product of L-arginine by the enzyme nitric oxide synthase, plays a pivotal role in the regulation of vascular homeostasis. Its complex interaction with the autocrine and paracrine systems, particularly angiotensin II, modulates vasoconstriction and vasodilatation as well as the architectural remodeling of the vascular bed. The major vascular hormones known to be involved are angiotensin II and endothelin-1. Upregulation of endothelin-1, a potent molecule, appears to be a consequence of the nitric oxide-angiotensin II imbalance that contributes to end-organ injury. Increased oxidative stress, common to different diseases including diabetes mellitus and hypertension, is also a determinant player in the interaction between angiotensin II and nitric oxide. The influence of a relative malfunction of the nitric oxide system on the vascular tone and vascular structure, and the effects of hypertension on this system, are discussed.
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Leclercq et al. (2002) conducted a review in Hypertension. A relative malfunction of the nitric oxide system and its imbalance with angiotensin II and endothelin-1 contribute to altered vascular tone, structural remodeling, and end-organ injury in hypertension.
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