There is sexual dimorphism in vascular reactivity and in receptor gene expression to Ang II in SHR. We conclude that estrogen modulates AT(1) and AT(2) receptor gene expression and that this might explain at least partially the lower blood pressure observed in female SHR.
Taken together, our findings demonstrate that male SHR presents higher superoxide anion concentration under basal condition than does female. An AT-1-dependent overexpression of the NAD(P)H-oxidase components may account for the sexual dimorphism in oxidative stress, and may play an important role in the noted gender differences on incidence of cardiovascular disease.
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