The inhibitory role of nitric oxide (NO) in the somatocardiac sympathetic C-reflex in anesthetized rats.

The role of nitric oxide (NO) in the two somatosympathetic reflex arcs, i.e. A- and C-reflexes, was examined using NO synthase (NOS) inhibitor in anesthetized rats. The A- and C-reflex components were recorded from a cardiac sympathetic efferent nerve and elicited by stimulation of myelinated A and unmyelinated C afferent fibers in the left tibial nerve. NG-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, when administered by either intrathecal (i.t.) or into the cisterna magna (i.c.m.) routes, augmented only the C-reflex in a dose-dependent manner. The effective i.t. dose of L-NAME to augment the C-reflex was approximately 1000 times the i.c.m. dose. NG-nitro-D-arginine methyl ester (D-NAME), an isomer of L-NAME, had no effect on either A- or C-reflexes, when administered i.c.m. Neither i.c.m. pre-treatment nor post-treatment with L-arginine, a NOS substrate, influenced either A- or C-reflexes, but i.c.m. pre-treatment with L-arginine abolished the facilitatory effect of L-NAME on the C-reflex. These results suggest that NO, synthesized in the brain stem, plays an inhibitory role in the central modulation of the somatocardiac sympathetic C-reflex. The possibility of movement of L-NAME to the brain stem from the spinal cord is discussed.