Role of nitric oxide in the nucleus tractus solitarii on the pressor response to static muscle contraction

Recently, it has been reported that static muscle contraction induces Fos-like immunoreactivity (FLI) in the nucleus tractus solitarii (NTS). Furthermore, NTS neurons have been found to contain nitric oxide synthase (NOS). The effects of nitric oxide (NO) on the cardiovascular responses to static muscle contraction in the NTS were determined in present study. Static contraction of the triceps surae muscle was induced by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in anesthetized cats. Immunocytochemical staining of the NTS for FLI and neuronal NADPH-diaphorase (NADPH-d, a nitric oxide synthase) was performed to evaluate the distribution of FLI cells within neurons of the NTS containing NOS. The results showed that NADPH-d positive fibers and FLI cells were co-distributed in the NTS of cats after muscle contraction. L-Arginine, the precursor of NO formation was microdialyzed into the NTS to determine the role of NO in the NTS on the blood pressure and heart rate responses during muscle contraction. Static muscle contraction increased mean arterial pressure (MAP) and heart rate (HR) 51±9 mm Hg and 18±3 beats/min, respectively. Forty minutes after microdialyzing 10 mM L-Arginine the pressor responses to muscle contraction was significantly attenuated. MAP increased 30±7 mm Hg (p<0.05), and HR increased 14±2 beats/min (p>0.05), whereas microdialyzing 10 mM D-Arginine into the NTS had no effect. Microdialysis of 2 mM L-NAME significantly blocked the effects of L-Arginine (p<0.05). These findings demonstrate that static muscle contraction activates neurons in close proximity with neuronal fibers containing NOS, and the increase of NOS activity during muscle contraction attenuates the pressor response. This finding indicates that NO plays a role in mediating the cardiovascular responses to static muscle contraction in the NTS.