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In ring preparations of human pulmonary artery contracted with noradrenaline (NA), the application of acetylcholine (ACh) enhanced the tension, and withdrawal produced a large relaxation which was sustained for about 10 min and required over 20 min for recovery; the latter relaxation appeared only in the endothelium-intact preparation. Indomethacin increased the amplitude of NA contractions, changed the ACh-induced contraction to relaxation, and inhibited the ACh-induced sustained relaxation. Nitroarginine increased the amplitude of NA and ACh-induced contractions, with no significant change in the ACh-induced sustained relaxation. These effects of indomethacin and nitroarginine were observed only in the endothelium-intact preparations. In NA-contracted preparations, exogenously applied prostaglandin I2 (PGI2) produced relaxation. Thus, in human pulmonary arteries, NA and ACh activities release vasodilator prostanoids and nitroarginine-sensitive EDRF from the endothelium, and initiate direct contractile actions to smooth muscle. The prostanoid-induced relaxation is sustained for a long time after the withdrawal of ACh stimulation and can be mimicked by exogenously-applied PGI2.

Endothelial Prostanoids Involved in the Relaxation Produced by Acetylcholine in the Human Pulmonary Artery.