| First Author | Sun D | Year | 1999 |
| Journal | Circ Res | Volume | 85 |
| Issue | 3 | Pages | 288-93 |
| PubMed ID | 10436172 | Mgi Jnum | J:57415 |
| Mgi Id | MGI:1344558 | Doi | 10.1161/01.res.85.3.288 |
| Citation | Sun D, et al. (1999) Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice. Circ Res 85(3):288-93 |
| abstractText | Nitric oxide and prostaglandins were shown to contribute to the endothelial mediation of flow-induced dilation of skeletal muscle arterioles of rats. Thus, we hypothesized that flow-induced dilation and its mediation are altered in gracilis muscle arterioles of mice deficient in the gene for endothelial nitric oxide synthase (eNOS-KO) compared with control wild-type (WT) mice. Gracilis muscle arterioles (approximate to 80 mu m) of male mice were isolated, then cannulated and pressurized in a vessel chamber. The increases in diameter elicited by increases in perfusate flow from 0 to 10 mu L/min were similar in arterioles from eNOS-KO (n = 28) and WT (n = 22) mice (approximate to 20 mu m at 10 mu L/min flow), Removal of the endothelium eliminated flow-induced dilations in vessels of both strains of mice. N-omega-nitro-L-arginine (L-NNA, 10(-4) mol/L) significantly inhibited flow-induced dilation in arterioles of WT mice by approximate to 51% but had no effect on responses of arterioles from eNOS-KO mice. Indomethacin (INDO, 10(-5) mol/L) inhibited flow- induced dilation of WT mice by approximate to 49%, whereas it completely abolished this response in arterioles of eNOS-KO mice, Simultaneous administration of INDO and L- NNA eliminated flow-induced responses in arterioles of WT mice. Dilations to carbaprostacyclin were similar at concentrations of 10(-8) and 3 x 10(-8) mol/L but decreased significantly at 10(-7) mol/L in arterioles of eNOS-KO compared with those of WT mice. These findings demonstrate that, despite the lack of nitric oxide mediation, flow-induced dilation is close to normal in arterioles of eNOS-KO mice because of an enhanced release of endothelial dilator prostaglandins and suggest that this vascular adaptation may contribute to the regulation of peripheral resistance in eNOS-KO mice. |
