Overproduction of nitric oxide (NO) by gene transduction of endothelial NO synthase (eNOS) in rostral ventrolateral medulla (RVLM), which is responsible for maintenance of vasomotor tone, reduces arterial pressure in spontaneously hypertensive rats (SHR). This NO-induced vasodepression, however, is not sustained and is followed by rebound hypertension. Because superoxide anion (O 2 . ) level is increased and synthesis or activity of mitochondrial manganese superoxide dismutase (SOD2) is reduced in RVLM during hypertension, we hypothesized that an interaction between NO and O 2 . in RVLM, using mitochondrial respiratory enzyme complexes (MRC) as the cellular target, contributes to those cardiovascular outcomes after eNOS gene transduction in SHR. The present study assessed this hypothesis using adenoviral vectors to overexpress eNOS (AdeNOS) and/or SOD2 (AdSOD2) in RVLM of SHR or normo- Nitric oxide (NO) is a gaseous molecule that plays an active role in central cardiovascular regulation (Zanzinger, 1999). One brain region in which NO is of pivotal importance in this regulatory machinery is the rostral ventrolateral medulla (RVLM) (Chan et al., 2001;Mayorov, 2005), which provides tonic sympathetic outflow for the maintenance of vasomotor tone (Dampney, 1994). Accumulating evidence suggests that NO deficiency in the RVLM may underlie sympathetic overexcitation (Kagiyama et al., 1998;Chan et al., 2003; TandaiHiruma et al., 2005) or impaired baroreflex regulation (Kishi et al., 2003) during hypertension. Accordingly, overproduction of NO by gene transduction of endothelial nitric-oxide
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