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- W1551135706 abstract "Mitochondrial depolarization promotes vasodilation of cerebral arteries; however, the contribution of neuronal nitric oxide synthase (nNOS) localized to the perivascular nerves to vasodilation has not been examined. Diameter measurements of endothelium-denuded isolated rat cerebral arteries showed that mitochondrial depolarization agents, BMS-191095 (BMS) and diazoxide (DZ) induced vasodilation (40±3% and 28±3%, respectively) that was sensitive to nNOS inhibition with 7-NI. Fluorescence studies on primary rat cortical neurons showed increased fluorescence to Fluo-4 and DAR in response to DZ and BMS indicating increased [Ca2+]i and NO generation, respectively. ESR studies using NO-specific spin trap (DETC) showed increased NO generation in response to DZ. Western blot studies of endothelium-denuded cerebral arteries as well as neurons treated with BMS and DZ displayed increased ratio of phosphorylated/total nNOS and Akt versus vehicle. Thus, mitochondrial depolarization of perivascular nerves and cortical neurons promotes NO generation by increasing [Ca2+]i and Akt-dependent phosphorylation of nNOS leading to cerebral vasodilation. This novel mechanism may link the neuronal metabolic activity to vasodilation. Grant Funding Source: Supported by NIH grant numbers HL-077731, HL-030260, HL093554, and HL-065380 (Busija)" @default.
- W1551135706 created "2016-06-24" @default.
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- W1551135706 date "2014-04-01" @default.
- W1551135706 modified "2023-10-14" @default.
- W1551135706 title "Mitochondrial depolarization of perivascular nerves induces cerebral vasodilation by neuronal nitric oxide synthase activation (1079.5)" @default.
- W1551135706 doi "https://doi.org/10.1096/fasebj.28.1_supplement.1079.5" @default.
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