Effects of Noradrenaline on Membrane Electrical Properties of Intrapulmonary Artery and Vein in the Rat

Transmembrane electrical responses produced by noradrenaline (NA) were recorded from intrapulmonary artery and vein muscles of the rat. In the artery, NA (above 1 nM) depolarized the membrane and, in high concentrations (above 1 μM), generated slow oscillatory potentials. The excitatory action of NA was antagonized by prazosin but not by yohimbine. The amplitude of electrotonic potentials was increased during the NA-induced depolarization. Separate stimulation of α1,- and β-adrenoceptors by NA potentiated and inhibited the high-K induced contraction, respectively. In the vein, NA produced a biphasic response, i.e., an initial transient (1-2 min) hyperpolarization followed by a slowly developing depolarization which required 15-20 min to reach the steady potential. The initial hyperpolarization was blocked by propranolol and the following depolarization by prazosin but not by yohimbine. Amplitude of electrotonic potential was decreased or increased during the NA-induced hyperpolarization and depolarization, respectively. The results provide evidence that in the intrapulmonary artery and vein of rats, stimulation of the α1-adrenoceptor depolarizes the membrane with associated increase in membrane resistance. Stimulation of β-adrenoceptors in the artery inhibited the muscle contraction, with no alteration of the membrane potential. The β-adrenoceptormediated hyperpolarization in the vein was accompanied by a decrease in membrane resistance.