THE ROLE OF NITRIC-OXIDE IN THE BARORECEPTOR-CARDIAC REFLEX IN CONSCIOUS WISTAR RATS

The role of nitric oxide (NO) in baroreceptor-cardiac reflex function was examined using a NO synthase inhibitor, N-omega-nitro-L-arginine m ethyl ester (L-NAME), in conscious Wistar rats. Mean arterial pressure (MAP) and heart period (HP) relationships were obtained by intravenou s injection of graded doses of phenylephrine and sodium nitroprusside (SNP). The baroreflex function was compared before and after L-NAME (1 0 mg/kg iv), L-NAME (10 mg/kg iv) followed by exogenous NO supplied as SNP (10-20 mu g . kg(-1). min(-1) iv), or SNP alone (20 mu g . kg(-1) . min(-1) iv). To find the effect of changing basal MAP on baroreflex function, the baroreflex function was also examined before and after p henylephrine (8 mu g . kg(-1). min(-1) iv) or L-NAME followed by conco mitant infusion of SNP and phenylephrine. L-NAME increased basal MAP a s well as HP from 104 +/- 1 to 141 +/- 2 mmHg and from 168 r 3 to 237 + 7 ms, respectively. L-NAME shifted the sigmoid curve in the directio n of higher MAP with a significant increase in the gain (gain: control 2.14 +/- 0.15 ms/mmHg, L-NAME 3.70 +/- 0.26 ms/mmHg, P < 0.001). L-NA ME together with SNP infusion did not significantly affect the gain, b asal MAP, or HP. Infusion of SNP alone shifted the sigmoid curve in th e direction of lower MAP but had no significant effect on the gain. An infusion of phenylephrine or L-NAME with concomitant infusion of SNP and phenylephrine increased basal MAP similarly as L-NAME alone did bu t had no significant effect on the gain. We conclude that endogenous N O tonically exerts a hypotensive effect and inhibits the gain of baror eceptor-cardiac reflex, and these roles of endogenous NO could be assu med by SNP.