Source: Hypertension  |  Posted 9 years ago

Basal nitric oxide production and release in hypertensive patients is improved with the AT(1) receptor blocker, valsartan, indicates recent research.

Endothelial function and nitric oxide availability are adversely affected by angiotensin II, say researchers at the University of Erlangen- Nurnberg, Germany. Consequently, they undertook an analysis of the AT(1) receptor blockade effect on endothelium -dependent vasodilation and basal nitric oxide (NO) production, and release in 60 patients with essential hypertension.

The patients, aged 53 ? 10 years, were randomised to six weeks of double-blind therapy with either valsartan (80mg), hydrochlorothiazide (25 mg) or a placebo, once daily.

Basal nitric oxide production and release was assessed using a forearm blood flow measurement response to intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA). In addition, endothelium-dependent vasodilation was assessed by measuring the forearm blood flow (FBF) response to intra-arterial administration of acetylcholine. Endothelium-independent changes in FBF were assessed with intra-arterial infusion of noradrenaline and sodium nitroprusside.

Following treatment with valsartan, the decreased forearm blood pressure responding to L-NMMA was augmented. However, no improvement was seen in patients who received either placebo or hydrochlorothiazide therapy.

Decreased forearm blood flow, which was induced by changes in L-NMMA following valsartan therapy. proved to be unrelated to changes in blood pressure. The researchers also noted that there was no substantial modification of the FBF response induced by intra-arterial infusion of acetylcholine, noradrenaline and sodium nitroprusside.

They concluded that since the blood pressure reduction with hydrochlorothiazide did not increase the availability of nitric oxide, the effect of AT1 receptor blockers were independent of the BP.