Nitric Oxide in Hypertension

• Published in: The journal of clinical hypertension (Greenwich, Conn.) Vol. 8; no. 12 Suppl 4; pp. 17 - 29
• Main Authors: Hermann, Matthias, Flammer, Andreas, Lüscher, Thomas F.
• Format: Journal Article
• Language: English
• Published: Three Parklands Drive, Darien, CT 06820‐3652 Le Jacq 01.12.2006
• Subjects: Adrenergic beta-Antagonists - pharmacology; Adrenergic beta-Antagonists - therapeutic use; Animals; Biological Availability; Blood Pressure - drug effects; Elasticity; Endothelium, Vascular - physiopathology; Endothelium-Dependent Relaxing Factors - pharmacology; Humans; Hypertension - physiopathology; Nitric Oxide - pharmacokinetics; Nitric Oxide - pharmacology; Nitric Oxide - physiology; Oxidative Stress - physiology; Renin-Angiotensin System - physiology; Review Paper; Sympathetic Nervous System - physiopathology; Vasomotor System - physiology
• DOI: 10.1111/j.1524-6175.2006.06032.x
• ISSN: 1524-6175

Hypertension is a major risk factor for cardiovascular disease, and reduction of elevated blood pressure significantly reduces the risk of cardiovascular events. Endothelial dysfunction, which is characterized by impairment of nitric oxide (NO) bioavailability, is an important risk factor for both hypertension and cardiovascular disease and may represent a major link between the conditions. Evidence suggests that NO plays a major role in regulating blood pressure and that impaired NO bioactivity is an important component of hypertension. Mice with disruption of the gene for endothelial NO synthase have elevated blood pressure levels compared with control animals, suggesting a genetic component to the link between impaired NO bioactivity and hypertension. Clinical studies have shown that patients with hypertension have a blunted arterial vasodilatory response to infusion of endothelium‐dependent vasodilators and that inhibition of NO raises blood pressure. Impaired NO bioactivity is also implicated in arterial stiffness, a major mechanism of systolic hypertension. Clarification of the mechanisms of impaired NO bioactivity in hypertension could have important implications for the treatment of hypertension.