BLOCKADE OF NEURONAL NITRIC-OXIDE SYNTHASE ALTERS THE BAROREFLEX CONTROL OF HEART-RATE IN THE RABBIT

In previous studies we used NG-nitro-L-arginine (L-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR ) and renal sympathetic nerve activity (RSNA). L-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or sli ghtly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Theref ore, in the present study the effects of the relatively selective neur onal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex co ntrol of HR and RSNA were investigated in rabbits. Intraperitoneal inj ection of 7-NI (50 mg/kg) had no effect on resting HR, MAP or RSNA. 7- NI significantly reduced the lower plateau of the HR-MAP baroreflex cu rve from 140 +/- 4 to 125 +/- 4 and from 177 +/- 10 to 120 +/- 9 beats /min in conscious and anesthetized preparations, respectively (P < 0.0 5). In contrast, there was no significant difference in the RSNA-MAP c urves before and after 7-NI administration in conscious or anesthetize d preparations. These data suggest that blockade of neuronal NO syntha se influences baroreflex control of HR but not of RSNA in rabbits.