Mechanism of action of alpha-adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

Abstract

1. The action of noradrenaline was studied in freshly dispersed cells of the rabbit portal vein using microelectrode techniques. 2. In normal physiological salt solution, the ionophoretic application of noradrenaline evoked an alpha-adrenoceptor-mediated depolarization and sometimes a beta-adrenoceptor-mediated hyperpolarization. Experiments were carried out in the presence of propranolol to study the membrane mechanism associated with alpha-adrenoceptor activation. 3. In the current clamp mode of recording, the equilibrium potential of the noradrenaline-evoked depolarization was -1.9 mV. The depolarization was brought about by an increase in membrane conductance. 4. Under voltage clamp conditions, noradrenaline produced an inward current with a reversal potential of -7 +/- 3 mV (mean +/- s.e. mean). 5. The relationship between the noradrenaline-induced inward current and clamp potential was non-linear. Depolarization enhanced the conductance elicited by noradrenaline. 6. Evidence is presented which suggests that an additional conductance mechanism (probably an increase in potassium conductance) is also evoked by alpha-adrenoceptor stimulation in dispersed cells of rabbit portal vein.