Acute production of vascular superoxide by angiotensin II but not by catecholamines

Objective To determine whether vascular superoxide is rapidly released by a ngiotensin II and is involved in vascular contraction. Design The effect of superoxide dismutase (SOD) on angiotensin II induced e levation of mean arterial blood pressure was measured. Subsequently, acute production of vascular superoxide by angiotensin II and its effect on isome tric tension were measured in rat aortic rings, The effects of catecholamin es were concomitantly measured, Methods and results The acute presser effects of angiotensin II were signif icantly reduced when rats were pretreated intravenously with SOD, When angi otensin II was added on aortic segments in the presence of Cypridina lucife rin analog, immediate elevations of chemiluminescence were observed which w ere inhibited by SOD. Furthermore, angiotensin II-induced elevations of iso metric tension in aortic rings were significantly reduced by SOD. The effec ts of epinephrine and norepinephrine were concomitantly measured and were n ot significant. Conclusions The acute superoxide producing effect is likely to be specific to angiotensin II, because such a significant modification of the effects w as not observed for catecholamines. Our results suggest that angiotensin II causes acute vascular superoxide production, which may be involved in the acute presser effects. J Hypertens 2000, 18:179-185 (C) Lippincott Williams & Wilkins.