Effect of ascorbic acid treatment on conduit vessel endothelial dysfunction in patients with hypertension

Hypertension is associated with low plasma ascorbic acid levels and impaire d endothelial function. Recent evidence suggests that increased vascular ox idative stress contributes to the pathophysiology of endothelial dysfunctio n and hypertension. We recently showed that chronic oral ascorbic acid ther apy lowers blood pressure in hypertensive patients. We hypothesized that it would also improve endothelial vasomotor function. In a randomized, double -blind, placebo-controlled study, we examined the effect of acute (2 g po) and chronic (500 mg/day for 1 mo) ascorbic acid treatment on brachial arter y flow-mediated dilation in 39 patients with hypertension. Compared with 82 age- and gender-matched normotensive controls, these patients had impaired endothelium-dependent, flow-mediated dilation of the brachial artery [8.9 +/- 6.1 vs. 11.2 +/- 5.7% (SD), P< 0.04]. After therapy, plasma ascorbic ac id concentrations increased acutely from 50 +/- 12 to 149 +/- 51 <mu>mol/l and were maintained at 99 +/- 33 mu mol/l with chronic treatment (both P< 0 .001). As previously reported, chronic ascorbic acid therapy reduced systol ic and mean blood pressure in these patients. However, acute or chronic asc orbic acid treatment had no effect on brachial artery endothelium-dependent , flow-mediated dilation or on endothelium-independent, nitroglycerin-media ted dilation. These results demonstrate that conduit vessel endothelial dys function secondary to hypertension is not reversed by acute or chronic trea tment with oral ascorbic acid. The effects of this treatment on resistance vessel vasomotor function warrant further investigation.