Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.

We examined the effect of angiotensin II–induced hypertension on vascular иO2Ϫ production and attempted to characterize the oxidase activated

S Rajagopalan; S Kurz; T Münzel; M Tarpey; B A Freeman; K K Griendling; D G Harrison


Scholarcy highlights

  • Angiotensin II exerts numerous effects on the cardiovascular system
  • We found that angiotensin II–induced hypertension is associated with increased vascular иO2Ϫ production and impaired vascular relaxations to acetylcholine, the calcium ionophore A23187, and nitroglycerin
  • The alteration of vascular relaxations to endogenous and exogenous nitric oxide was likely, at least in part, due to the increase in vascular иO2Ϫ production, as it was partially corrected by augmenting vascular superoxide levels with liposome-entrapped superoxide dismutase
  • In contrast to the effect of angiotensin II infusion, NE infusion, which produced a similar degree of hypertension, did not increase vascular иO2Ϫ production and did not alter endothelium-dependent vascular relaxation
  • Recent observations by Griendling et al reveal that angiotensin II activates an NADH/NADPH oxidase in cultured vascular smooth muscle cells in a dose- and timedependent fashion
  • The present studies add to these recent observations by demonstrating that angiotensin II can exert this effect in vivo, and that this increase in иO2Ϫ production may contribute to alterations in endothelium-dependent vascular relaxation and responses to exogenous nitrovasodilators in the intact vessel
  • These findings are compatible with the concept that hypertension per se is not a stimulus for increased иO2Ϫ production, and that conditions in which circulating or local levels of angiotensin II are elevated may have unique effects on the vessel wall, independent of elevating blood pressure

Need more features? Save interactive summary cards to your Scholarcy Library.