1. Strips of rabbit main pulmonary artery (RMPA) were used to study the effects of several agonists on tension development and membrane potential of the vascular smooth muscle cells.
2. The following α-adrenoceptor agonists were employed: methoxamine and St 587 (α1-selective), B-HT 920 (α2-selective) and clonidine, which stimulates preferentially α2-adrenoceptors. By the use of the selective antagonists prazosin and yohimbine it was not possible to differentiate convincingly between α1- and α2-adrenoceptors in the RMPA. Methoxamine and B-HT 920 produced depolarization of similar magnitude of the membrane of the vascular smooth muscle cells. In spite of these results, which point to a uniform α-adrenoceptor in the RMPA, contractions to α1-and α2-agonists differed in some important aspects.
3. Contractions in response to α2-agonists were highly susceptible to the inhibitory effects of calcium withdrawal and calcium antagonists whereas contractions to α1-agonists were much less so. Reduction of the membrane potential of the vascular cells by K+ at 12 mmol/l had no effect on the concentration-contraction curve of methoxamine but shifted that of B-HT 920 to the left. Conversely hyperpolarization of the membrane of the vascular smooth muscle cells by strychnine totally suppressed contraction to B-HT 920 and caused only a rightward shift of the concentration-contraction curve of methoxamine and St 587.
4. Interaction of α1- and α2-agonists with an apparently uniform α-adrenoceptor induces in the RMPA contraction which seems to be triggered by different membrane processes.
