[Effect of manganese and verapamil on electrical and contractile responses of pulmonary artery smooth muscle induced by noradrenaline and histamine].

Action of noradrenaline and histamine on the resting potential, membrane resistance and contractility of rabbit pulmonary artery muscle cells was investigated in normal and Ca-blockers (manganese and verapamil)-containing Ringer-Lock solutions. It was shown that catecholamine and histamine induced depolarization by different mechanisms. Thus, noradrenaline action is accounted for by the decreased membrane permeability to potassium ions, while the histamine-induced depolarization is a consequence of sodium and, probably, chlorine permeability. The contraction induced by the transmitters is activated primarily by the extracellular calcium ions entering the cells by two ways: via chemosensitive Ca-channels activated by adrenergic and histaminergic receptors or via potential-dependent slow Ca-channels activated by the transmitter-induced membrane depolarization. It is not excluded that during activation of muscle cells by the transmitters part of calcium is release from both intramembrane and intracellular stores.