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1 Department of Physiology, New York Medical College, Valhalla, New York 10595; and 2 University of Texas Southwestern Medical Center, Dallas, Texas 75235
Flow-induced dilation of
gracilis muscle arterioles was examined in both genders of control rats
and rats chronically treated with
N
-nitro-L-arginine methyl ester
(L-NAME). After L-NAME treatment (4 wk),
systolic blood pressure was significantly increased compared with
control, whereas the plasma concentration of nitrate/nitrite was
significantly reduced. Isolated and pressurized arterioles dilated
significantly in response to increases in flow (0-25 µl/min). Flow-induced dilation was comparable in arterioles of control and
L-NAME-treated rats but was significantly greater in female than in male rats. L-NAME + indomethacin, which
abolished flow-induced dilation in arterioles of male control rats,
inhibited the dilation by only ~75% in female control rats. The
residual portion of the response was eliminated by additional
administration of miconazole, an inhibitor of cytochrome
P-450. Indomethacin did not affect the dilation in female
L-NAME-treated rats but completely inhibited the response
in male L-NAME-treated rats. The indomethacin-insensitive, flow-induced dilation in female L-NAME-treated
arterioles was abolished by miconazole,
6-(2-proparglyoxyphenyl)hexanoic acid, or charybdotoxin. Thus an
augmented release of endothelial prostaglandins accounts for the
preserved flow-induced dilation in arterioles of male rats, whereas a
metabolite of cytochrome P-450 is responsible for the
maintenance of flow-induced dilation in female rats, suggesting important differences in the adaptation of the endothelium of arterioles from male and female rats to the lack of nitric oxide (NO) synthesis.
NO synthesis; hyperpolarizing factor; cytochrome P-450 metabolites; potassium channels
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