Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

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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 α-adrenoceptor-mediated depolarization and sometimes a β-adrenoceptor-mediated hyperpolarization. Experiments were carried out in the presence of propranolol to study the membrane mechanism associated with α-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 α-adrenoceptor stimulation in dispersed cells of rabbit portal vein.

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