Release of nitric oxide after acute hypertension

We have shown that NO production, assessed by measuring changes in plasma n itrate concentration, is downregulated when blood pressure falls. This stud y intended to determine first, whether NO-derived plasma nitrate varies in response to increases in blood pressure induced by different mechanical and pharmacologic stimuli, including angiotensin II and catecholamines; and se cond, specifically to study the interaction between angiotensin II and NO p roduction. An intravenous infusion (4-10 min) of norepinephrine (7.5 mu g/k g/min), phenylephrine (30 mu g/kg/min), or angiotensin II (0.3 and 3 mu g/k g/min) caused hypertension accompanied by an increase in plasma nitrate, as assessed by high-performance capillary electrophoresis. Mechanical hyperte nsion elicited by aortic occlusion also was accompanied by an increase in p lasma nitrate. Angiotensin II (0.03, 0.3, and 3 mu g/kg/min, 10 min) dose-d ependently increased blood pressure. The intermediate and high dose, but no t the low dose, of angiotensin II increased plasma nitrate concentration. N -G-nitro-L-arginine methyl ester (L-NAME) lowered the basal concentration o f plasma nitrate, abolished the increase in plasma nitrate elicited by angi otensin II and norepinephrine, and potentiated the presser effect of the lo w dose of angiotensin II, although this dose did not increase NO production . L-NAME also potentiated the presser effects of the intermediate dose of a ngiotensin II. This study demonstrates that an augmented systemic productio n of NO, measured as an increase in plasma nitrate, takes place after acute hypertension. The results of this study suggest that an increase in NO gen eration occurs when angiotensin II hypertension exceeds a certain limit, be low which the basal production of NO is sufficient to compensate the vasoco nstriction.