Nitric oxide (NO)-mediated, vasodilator nerve function and its susceptibility to calcium antagonists

Our pharmacological and immunohistochemical studies have demonstrated that nitric oxide (NO) or a substance that liberates NO plays a crucial role in the neurogenic relaxation of isolated cerebral arteries of dog and monkey. Relaxation caused by nerve stimulation by nicotine or electrical pulses in dog cerebral arteries without the endothelium were attenuated by Cd2+, a non-selective Ca2+ channel antagonist. Increase in cyclic GMP by nicotine was also suppressed by Cd2+, but not by nicardipine. Treatment with capsaicin did not influence the relaxant responses of the endothelium-denuded cerebral arteries to nerve stimulation. These results suggest that neurotransmission in vasodilator nerves innervating dog cerebral arteries is mainly mediated by NO, synthesized by an NO synthase which is activated by Ca2+ influx through non-L-type Ca2+ channel, but not by vasodilator peptides.