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Noradrenaline Release in the Human Pulmonary Artery is Modulated by Presynaptic α2Adrenoceptors

Summary: We used strips of human pulmonary arteries from patients undergoing surgery for lung tumor to investigate whether or not this human tissue (like that of the rabbit) is endowed with inhibitory presynaptic α2-ad-renoceptors. The strips were incubated with incubated with [3H]noradrenaline and subsequently superfused with physiological salt solution containing cocaine, corticosterone, and propranolol. The electrically (2 Hz) evoked overflow of tritium consisted of 89% unmetabolized [3H]noradrenaline and was abolished by tetrodotoxin or omission of Ca2+ from the superfusion fluid. Unlabeled noradrenaline, adrenaline, and the preferential α2-adrenoceptor agonists B-HT 920, α-methylnoradrenaline, and clonidine concentration dependently inhibited the evoked overflow (maximum effect of clonidine lower than that of the other compounds); the α2-selective agonist methox-amine was ineffective. The α2-adrenoceptor antagonists BDF 6143 and rauwolscine facilitated the evoked over-flow; the α2-selective antagonist prazosin was ineffective. The concentration-response curve of B-HT 920 for its inhibitory effect on evoked overflow was shifted to the right by rauwolscine. It is concluded that the sympathetic nerve fibres of the human pulmonary artery possess presynaptic α2-adrenoceptors. Stimulation-evoked release of noradrenaline is inhibited by activation and facilitated by blockade of these receptors.