Abstract
The role of perivascular nerves in the mitochondria-mediated cerebral artery vasodilation has not been studied. Our objective was to examine the role of neuronal nitric oxide synthase (nNOS) localized to the perivascular nerves in mitochondria-dependent vasodilation. Changes in the diameter of endothelium denuded isolated rat cerebral arteries were determined in response to mitochondrial depolarization agents, BMS-191095 (BMS) and diazoxide (DZ). BMS and DZ induced endothelium-independent vasodilation that was diminished by nNOS inhibitor, 7-nitroindazole (7-NI) and Na+ channel blocker, tetradotoxin. Estimation of NO generation in primary rat cortical neurons by diaminorhodamine-4M (DAR), a NO-sensitive fluoroprobe, showed enhanced fluorescence in response to BMS and DZ compared to vehicle, that was abolished by NOS inhibitors, Nω-nitro-L-arginine methyl ester and 7-NI. Thus, mitochondrial depolarization of perivascular neurons promotes NO generation by nNOS activation leading to cerebral vasodilation. This novel mechanism may link the neuronal metabolic activity to vasodilation.
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