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Previously we found that flow-induced arteriolar dilation in male spontaneously hypertensive rats (SHR) is significantly impaired, due to the absence of the nitric oxide (NO)-mediated portion of the response, resulting in an elevation of maintained wall shear stress. Since estrogen has been shown to affect NO-mediated responses, we hypothesized that in female SHR (fSHR) the NO-mediated portion of flow-induced responses is preserved. Gracilis muscle arterioles (approximately 45 to 55 microm) from 12-week-old fSHR, ovariectomized fSHR (OV fSHR), or ovariectomized and supplemented with estrogen fSHR (OVE fSHR) were isolated, cannulated, and pressurized at 80 mm Hg of perfusion pressure. Arteriolar dilations elicited by step increases in perfusate flow from 0 to 25 microL/min were significantly less (by approximately 30%) in OV fSHR compared with fSHR and OVE fSHR (delta19.4+/-1.5 versus 26.0+/-0.9 and 26.8+/-2.0 microm, respectively at maximum flow rate). Inhibition of prostaglandin synthesis with indomethacin elicited a approximately 50% reduction in flow-dependent dilation in all three groups of rats. N(omega)-nitro-L-arginine (L-NNA) significantly inhibited flow-induced responses in arterioles of fSHR and OVE fSHR (by approximately 50%) but not in those of OV fSHR. Constrictions to norepinephrine (10(-7)-3 x 10(-7) mol/L) were significantly greater (up to approximately 40%) in arterioles of OV fSHR compared with those of fSHR and OVE fSHR; these differences, however, were abolished in the presence of L-NNA. In conclusion, estrogen seems to preserve the NO-mediated portion of flow/shear stress-induced dilation in female hypertensive rats resulting in a lower maintained wall shear stress in female than in male SHR. The lower wall shear stress may contribute to the mechanisms by which estrogen lowers systemic blood pressure and the incidence of cardiovascular diseases in women.

Estrogen Preserves Regulation of Shear Stress by Nitric Oxide in Arterioles of Female Hypertensive Rats