We examined the role of central nitric oxide (NO) in the baroreceptor reflex in conscious rabbits. Intracerebroventricular infusion of 20 μmol of N(ω)-nitro-L-arginine methyl ester (L-NAME) to block central NO resulted in increases in arterial pressure, renal sympathetic nerve activity (RSNA), and plasma catecholamine levels, and the pressor response was suppressed by pretreatment with pentolinium (5 mg/kg iv). On the other hand, a subpressor dose of intracerebroventricular L-NAME (10 μmol/h) caused significant increases in baroreflex sensitivities assessed by RSNA and heart rate compared with vehicle infusion [maximum gain: -18.2 ± 0.9 vs. -9.6 ± 0.9%/mmHg (P < 0.001) and -14.3 ± 2.3 vs. -5.7 ± 0.4 beats · min-1 · mmHg-1 (P < 0.05), respectively]. Conversely, an intracerebroventricular infusion of Et2N[N(O)NO]Na, an NO donor (1 μmol/h) significantly attenuated the baroreflex sensitivities. However, intracerebroventricular infusion of N(ω)-nitro-D-arginine methyl ester (10 μmol/h), an enantiomer of L-NAME, failed to alter the baroreflex sensitivities. These results suggest that 1) the pressor response induced by inhibition of central NO synthesis is mainly mediated by the enhanced sympathetic outflow and 2) central NO attenuates the baroreflex control of RSNA and heart rate in conscious rabbits.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||4 43-4|
|Publication status||Published - Apr 1998|
All Science Journal Classification (ASJC) codes
- Physiology (medical)