Electrical responses evoked by perivascular nerve stimulation were recorded from rat small intrapulmonary artery with the microelectrode technique. Nerve stimulation with a single pulse produced an excitatory junction potential that was insensitive to phentolamine, propranolol, atropine, ketanserin, mepyramine, and guanethidine but was abolished by tetrodotoxin. Treatment with reserpine in vivo or with 6-hydroxydopamine in vitro had no significant effect on the amplitude of the junction potentials. In the mesenteric arteries from the same rats, these procedures led to the inhibition of the junction potentials, confirming adequate functional sympathectomy. Low concentrations of α,β-methylene ATP attenuated the amplitude of the excitatory junction potential without changing the membrane potential. The membrane depolarization induced by ATP was inhibited by α,β-methylene ATP, but those induced by norepinephrine or serotonin were not. It is concluded that the excitatory junction potential in rat pulmonary artery results from the release of a nonadrenergic, noncholinergic neurotransmitter from perivascular nerves that are not sympathetic and that the most likely transmitter is ATP. Such neurotransmisssion may play a role in the regulation of regional pulmonary blood flow.
|American Journal of Physiology - Heart and Circulatory Physiology
|Published - Jan 1 1988