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 methyl ester (L-NAME), in conscious Wistar rats. Mean arterial pressure (MAP) and heart period (HP) relationships were obtained by intravenous injection of graded doses of phenylephrine and sodium nitroprusside (SNP). The baroreflex function was compared before and after L-NAME (10 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 phenylephrine (8 mu g . kg(-1). min(-1) iv) or L-NAME followed by concomitant infusion of SNP and phenylephrine. L-NAME increased basal MAP as 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 direction 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-NAME together with SNP infusion did not significantly affect the gain, basal MAP, or HP. Infusion of SNP alone shifted the sigmoid curve in the 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 but had no significant effect on the gain. We conclude that endogenous NO tonically exerts a hypotensive effect and inhibits the gain of baroreceptor-cardiac reflex, and these roles of endogenous NO could be assumed by SNP.