Relaxation of Rat Main Pulmonary Artery to Electrical Stimulation: Role of Nitric Oxide

The present study was undertaken to determine participation of nitric oxide (NO) in noradrenergic, noncholinergic relaxation induced by electrical field stimulation (EFS) of perivascular nerves in isolated rat main pulmonary artery and its extralobar branches. Electrical field stimulation caused a frequency-dependent relaxation of main pulmonary artery of the rat precontracted with phenylephrine. NG-nitro-L-arginine, inhibitor of nitric oxide synthase, inhibited the relaxation of pulmonary artery. Tetrodotoxin in concentration which was sufficient to block the contractile responses induced by EFS was unable to influence the relaxation response of phenylephrineprecontracted artery. These results suggest that EFS-induced relaxation in main pulmonary artery is mediated by NO mainly of nonneurogenic origin. 7-nitroindazole, neuronal NO synthase inhibitor, as well as capsaicin, a neurotoxin for sensory nerves, moderately attenuated the relaxant responses induced by EFS indicating that at least part of relaxation is mediated by neurally derived NO. The extension of EFS-induced relaxation in main pulmonary artery of spontaneously hypertensive rats was smaller than in normotensive control rats. The results suggest that EFS-induced release of NO contributes to maintaining the low resistance in lung circulation.