| First Author | Demchenko IT | Year | 2002 |
| Journal | Circ Res | Volume | 91 |
| Issue | 11 | Pages | 1031-7 |
| PubMed ID | 12456489 | Mgi Jnum | J:133980 |
| Mgi Id | MGI:3784737 | Doi | 10.1161/01.res.0000043500.03647.81 |
| Citation | Demchenko IT, et al. (2002) Regulation of the brain's vascular responses to oxygen. Circ Res 91(11):1031-7 |
| abstractText | The mechanism of oxygen-induced cerebral vasoconstriction has been sought for more than a century. Using genetically altered mice to enhance or disrupt extracellular superoxide dismutase (EC-SOD, SOD3), we tested the hypothesis that this enzyme plays a critical role in the physiological response to oxygen in the brain by regulating nitric oxide (NO*) availability. Cerebral blood flow responses in these genetically altered mice to changes in PO2 demonstrate that SOD3 regulates equilibrium between superoxide (*O2-) and NO*, thereby controlling vascular tone and reactivity in the brain. That SOD3 opposes inactivation of NO* is shown by absence of vasoconstriction in response to PO2 in the hyperbaric range in SOD3+/+ mice, whereas NO-dependent relaxation is attenuated in SOD3-/- mutants. Thus, EC-SOD promotes NO* vasodilation by scavenging *O2- while hyperoxia opposes NO* and promotes constriction by enhancing endogenous *O2- generation and decreasing basal vasodilator effects of NO*. |
