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Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein
Author(s) -
Byrne N.G.,
Large W.A.
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11550.x
Subject(s) - depolarization , hyperpolarization (physics) , membrane potential , biophysics , conductance , chemistry , reversal potential , current clamp , voltage clamp , propranolol , stimulation , electrophysiology , medicine , endocrinology , patch clamp , biology , stereochemistry , mathematics , combinatorics , nuclear magnetic resonance spectroscopy
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.