It is well known that hypertension attenuate endothelium-dependent vasodilator response. And this finding is closely related to the development of atherosclerosis. Recently it is reported that the expression of NADPH-dependent oxidase is increased in angiotensin-induced hypertension model and superoxide (O₂) produced from that might contribute to the development of vascular diseases. The possible mechanism is the degradation of endothelium-derived NO by O₂. We hypothesized that SOD prevents endothelial dysfunction via prevention of the degradation of endothelium-derived NO.

We made renovascular hypertension model by constricting abdominal aorta just above the left renal artery of Sprague-Dawley female rats. The descending thoracic aorta was stuied in the organ chambers using acetylcholine as an endothelium-dependent vasodilator with or without pretreatment of SOD.

Blood pressures of all 14 rats were significantly increased (174/123 mmHg, mean 146 mmHg). The residual tensions of the vessels precontracted by phenylephrine were similar in both groups (15.04±19.53 % in SOD group vs 11.84±18.57% in non-SOD group, p=.66).

The endothelial dysfunctions in the rat aorta with renovascular hypertension were not improved by SOD. There is no acute effect of SOD on endothelial function in high renin/angiotensin state.