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* To whom correspondence should be addressed. E-mail: frank-faraci{at}uiowa.edu.
ABSTRACT We tested the hypothesis that the mitochondrial form of superoxide dismutase (Mn-SOD) protects the cerebral vasculature. Basilar arteries (baseline diameter ~140 microns) from mice were isolated, cannulated and pressurized in order to measure vessel diameter. In arteries from C57BL6 mice preconstricted with U-46619, acetylcholine (Ach, an endothelium-dependent vasodilator) produced dilation that was similar in male and female mice and abolished by an inhibitor of nitric oxide synthase. Vasodilation to Ach was not altered in heterozygous male or female MnSOD deficient (+/-) mice compared to wild-type littermate controls (Mn-SOD +/+). Constriction of the basilar artery to arginine vasopressin, but not KCl or U-46619, was increased in Mn-SOD +/- mice (P<0.05) and this effect was prevented by Tempol, a scavenger of superoxide. We also examined responses of cerebral (pial) arterioles (branches of the middle cerebral artery, control diameter ~30 microns) to Ach in anesthetized mice using a cranial window. Responses to Ach, but not nitroprusside (an endothelium-independent agonist), were reduced (P<0.05) in cerebral arterioles in Mn-SOD +/- mice and this effect was prevented by Tempol. Thus, these are the first data on the role of Mn-SOD in cerebral circulation. In the basilar artery, Ach produced NO-mediated dilation that was similar in male and female mice. Under normal conditions in cerebral arteries, responses to Ach were not altered but constrictor responses were selectively enhanced in Mn-SOD +/- mice. In the cerebral microcirculation, there was superoxide-mediated impairment of responses to Ach.
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