| First Author | Huang A | Year | 2002 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 282 |
| Issue | 2 | Pages | H429-36 |
| PubMed ID | 11788389 | Mgi Jnum | J:75602 |
| Mgi Id | MGI:2177112 | Doi | 10.1152/ajpheart.00501.2001 |
| Citation | Huang A, et al. (2002) Neuronal NOS-dependent dilation to flow in coronary arteries of male eNOS-KO mice. Am J Physiol Heart Circ Physiol 282(2):H429-36 |
| abstractText | Flow-induced dilation was examined in isolated coronary arteries of endothelial nitric oxide (NO) synthase knockout mice (eNOS-KO) and wild-type (WT) mice. The basal tone of arteries (percentage of passive diameter) was significantly greater in eNOS-KO than in WT mice; their flow-induced dilations, however, were similar. Endothelial removal eliminated the dilations in vessels of both strains of mice. In arteries of WT mice, N(omega)-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or indomethacin (10(-5) M) alone, inhibited flow-induced dilation by approximately 50%, whereas their simultaneous administration abolished the responses. In arteries of eNOS-KO mice, flow-induced dilation was inhibited by approximately 40% with L-NAME. The residual portion (60%) of the response was eliminated by the additional administration of indomethacin. 7-Nitroindazole (10(-4) M) attenuated flow-induced dilation by approximately 40% in arteries of eNOS-KO mice, but did not affect responses in those of WT mice. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (3 x 10(-5) M) inhibited the L-NAME/7-nitroindazole-sensitive portion of the responses in arteries of eNOS-KO mice. Immunohistochemical evidence confirms the presence of neuronal NOS (nNOS) in the arterial endothelium of eNOS-KO mice. In conclusion, nNOS-derived NO, via activation of cGMP, together with prostaglandins, maintains flow-induced dilation in coronary arteries of male eNOS-KO mice. |
