Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 280, Issue 6, Pages H2456-H2461Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.280.6.H2456
Keywords
NO synthesis; hyperpolarizing factor; cytochrome P-450 metabolites; potassium channels
Funding
- NHLBI NIH HHS [HL-43023, HL-46813] Funding Source: Medline
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Flow-induced dilation of gracilis muscle arterioles was examined in both genders of control rats and rats chronically treated with N-omega-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 mul/ 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 similar to 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.
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