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) inhibit or 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. N-G-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, wh en administered by either intrathecal (i.t.) or into the cisterna magn a (i.c.m.) routes, augmented only the C-reflex in a dose-dependent man ner. The effective i.t. dose of t-NAME to augment the C-reflex was app roximately 1000 times the i.c.m. dose. N-G-nitro-D-arginine methyl est er (D-NAME), an isomer of L-NAME, had no effect on either A- or C-refl exes, when administered i.c.m. Neither i.c.m. pre-treatment nor post-t reatment with L-arginine, a NOS substrate, influenced either A- or C-r eflexes, but i.c.m, pre-treatment with L-arginine abolished the facili tatory effect of L-NAME on the C-reflex. These results suggest that NO , synthesized in the brain stem, plays an inhibitory role in the centr al modulation of the somatocardiac sympathetic C-reflex. The possibili ty of movement of L-NAME to the brain stem from the spinal cord is dis cussed.