ROLE OF NITRIC-OXIDE IN REGULATION OF BARORECEPTOR REFLEX

The possible role of nitric oxide (NO) on modulating sympathetic nerve activity through its action on baroreceptor reflex are was investigated. L-Arginine, a precursor of NO, and N-G-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, were separately infused intravenously in increasing doses in 126 pentobarbital-anesthetized rabbits. Mean arterial pressure (MAP), heart rate (HR), aortic nerve activity (ANA), cervical (CSNA) and renal sympathetic nerve activities (RSNA) were recorded. L-Arginine infusion decreased MAP (P < 0.05), ANA (P < 0.05), CSNA (P < 0.05) and RSNA (P < 0.05) without changes in HR. Infusion of D-arginine, an enantiomer of L-arginine, and simultaneous infusion of L-arginine and L-NMMA, did not elicit such changes. L-NMMA infusion increased MAP (P < 0.05) and ANA (P < 0.05) and decreased HR (P < 0.05), while it tended to increase CSNA and RSNA without significance. Infusion of L-arginine or L-NMMA did not alter the slope of ANA, CSNA, RSNA, or HR in relation to MAP, These results suggest that NO modulates efferent sympathetic nerve activity, not by altering the afferent or efferent limbs of the baroreceptor reflex are, but by interacting with the sympathetic pathway in the central nervous system.