Role of angiotensin II in modulating the hemodynamic effects of nitric oxide synthesis inhibition

This study examined the role of ANG II in modulating the increase of hemato crit and vascular permeability that follows nitric oxide (NO) synthesis blo ckade, that are contributing to the decrease in cardiac index (CI) in consc ious, chronically catheterized rats. Pretreatment with losartan attenuated the N-omega-nitro-L-arginine methyl ester (L-NAME)-induced increase in tota l peripheral resistance by 26% and also blunted the fall in CI (28%) and st roke volume. L-NAME produced an increase in hematocrit (4.5%) and in I-125- labeled albumin content in the heart and small intestine in untreated rats, but the increase was prevented in rats pretreated with losartan. Furthermo re, L-NAME induced a transient increase of plasma protein concentration and tissue intestinal blood flow, which was abolished in rats given losartan. The results of the present study indicate that the systemic hemodynamic res ponses, the fall in plasma volume, and the increase in albumin escape obser ved after inhibition of NO synthesis are in part the consequence of unmaski ng the actions of endogenous ANG II. These data suggest a physiological rol e for NO by restraint of the vascular actions of the renin-angiotensin syst em.