Cardiovascular responses to angiotensins I and II in normotensive and hypertensive rats; effects of NO synthase inhibition or ET receptor antagonism

1 We compared the cardiovascular responses to angiotensins (I and II), and any possible modulatory influences thereupon of nitric oxide (NO) or endoth elin (ET) in conscious male, normotensive, Hannover Sprague-Dawley (SD) rat s, and hypertensive, heterozygous ((mRen-2)27), transgenic (TG) rats. 2 The presser effects of angiotensin I or of angiotensin II were not consis tently different in SD and TG rats. The accompanying absolute reductions in renal and mesenteric vascular conductances were smaller in TG rats, but pr obably due to the baseline vasoconstriction in those animals. 3 Inhibition of NO synthase with L-NAME had no significant effects on the p resser responses to angiotensin I or angiotensin II in either SD or TG rats . L-NAME reduced the absolute, but not percentage, reductions in renal and mesenteric vascular conductances in response to angiotensin I and angiotens in II. L-NAME abolished the hindquarters vasodilator effects of angiotensin I and angiotensin II in both strains of rat. 4 ET receptor antagonism (with SB209670) had no significant influence on th e presser or renal or mesenteric vasoconstrictor effects of angiotensin II in SD rats. In TG rats, the presser responses to angiotensin II were unaffe cted by SB209670; the accompanying falls in renal and mesenteric vascular c onductances were enhanced in absolute, but not in percentage terms. 5 These results provide no evidence for a buffering action of NO, or a modu latory influence of ET, on the presser or vasoconstrictor effects of angiot ensin I and/or angiotensin II in SD rats. Furthermore, there is no evidence for an altered sensitivity to angiotensin I or angiotensin II, and no evid ence for a differential modulatory influence of either NO or ET in TG, comp ared to SD, rats.