| First Author | Britto-Júnior J | Year | 2023 |
| Journal | Nitric Oxide | Volume | 138-139 |
| Pages | 26-33 | PubMed ID | 37269938 |
| Mgi Jnum | J:354817 | Mgi Id | MGI:7715009 |
| Doi | 10.1016/j.niox.2023.06.001 | Citation | Britto-Junior J, et al. (2023) The importance of the endothelial nitric oxide synthase on the release of 6-nitrodopamine from mouse isolated atria and ventricles and their role on chronotropism. Nitric Oxide 138-139:26-33 |
| abstractText | 6-nitrodopamine (6-ND) is released from rat isolated atria, where it acts as a potent positive chronotropic agent. The release of 6-ND from rat isolated atria and ventricles is significantly reduced when pre-incubated with l-NAME, and the release was not affected by tetrodotoxin pre-treatment, indicating that in the heart, the origin of 6-ND is not neurogenic. Since l-NAME inhibits all three isoforms of NO synthase, it was investigated the basal release of 6-ND from isolated atria and ventricles from nNOS(-/-), iNOS(-/-) and eNOS(-/-) mice of either sex. The release of 6-ND was measured by LC-MS/MS. There were no significant differences in the 6-ND basal release from isolated atria and ventricles from male control mice, as compared to female control mice. The 6-ND release from atria obtained from eNOS(-/-) mice was significantly reduced when compared to atria obtained from control mice. The 6-ND release in nNOS(-/-) mice was not significantly different compared to control animals whereas the 6-ND release from atria obtained from iNOS(-/-) mice was significantly higher when compared to control group. Incubation of the isolated atria with l-NAME caused a significant decrease in the basal atrial rate of control, nNOS(-/-), and iNOS(-/-) mice, but not in eNOS(-/-) mice. The results clearly indicate that eNOS is the isoform responsible for the synthesis of 6-ND in the mice isolated atria and ventricles and supports the concept that 6-ND is the major mechanism by which endogenous NO modulates heart rate. |
