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NADPH oxidase, superoxide overproduction and nitric oxide bioavailability in essential hypertension.

The multiple inter-relationships that link hypertension, angiotensin II, oxidative stress and nitric oxide (NO) systems clearly suggest that angiotensin II, oxidative stress and NO comprise a homeostatic system that regulates both vascular function and structure [1]. A major nexus of these inter-relationships is via the effect of angiotensin II on NADH/NADPH oxidase. Angiotensin II upregulates this oxidase [2] and the resulting increased free radical production reacts with NO to reduce its bioavailability, thereby leading to impaired NO-dependent vasodilation and increased vascular oxidative stress. These then drive hypertension and remodelling [1].