THE EFFECTS OF INTRINSIC NITRIC-OXIDE ON CARDIAC NEURAL REGULATION INCATS

In this study, we aimed to elucidate the effects of intrinsic nitric o xide (NO) on cardiac neural regulation. Twenty-two cats were anestheti zed with 1.5% isoflurane and allocated to Group I (intact; n = 7), Gro up D (denervated baroreceptors and vagi; n = 8), or Group B (autonomic blockade with IV hexamethonium, propranolol, and atropine; n = 7). Ca rdiac sympathetic nerve activity (CSNA), mean arterial pressure (MAP), sinus heart rate (HR), and A-H and H-V intervals during pacing (150 b pm) were measured before and after IV administration of a NO synthase inhibitor, N-G-nitro-L-arginine (L-NNA, 30 mg/kg) and after reversal w ith an excessive dose of L-arginine (300 mg/kg), before and during int ermittent electrical stimulation of the posterior hypothalamus. L-NNA significantly increased MAP in Groups I and B, but not in Group D. L-N NA significantly decreased HR and lengthened A-H in Group I,but not in other groups. L-arginine further decreased HR and lengthened A-H unex pectedly. The reasons for these findings could not be determined in th is study. L-NNA did not change CSNA. Hypothalamic stimulation did not potentiate L-NNA-induced changes in CSNA, hemodynamic variables, and a trioventricular conduction. In conclusion, intrinsic NO may modulate a trioventricular conduction and sinus rate through a vagal cholinergic, rather than a nonautonomic mechanism. Implications: Elucidating the r oles of intrinsic nitric oxide (NO) on cardiac neural regulation is im portant. In intact, vagotomized, and baroreceptor-denervated or pharma cologically autonomic blockaded cats, an NO synthesis inhibitor was ad ministered, and atrioventricular conduction and cardiac sympathetic ne ural discharge were measured. The results suggest a vagal cholinergic mechanism of intrinsic NO.