Microelectrode study on the ionic mechanisms which contribute to the noradrenaline‐induced depolarization in isolated cells of the rabbit portal vein

Abstract

1 Experiments were carried out to determine the identity of the ionic mechanisms which contribute to the noradrenaline-evoked depolarization recorded with microelectrodes in freshly dispersed rabbit portal vein cells. 2 In normal physiological salt solution with microelectrodes containing 1 m NaCl the reversal potential (E_r) of the noradrenaline-induced response was −7.6 ± 2.9 mV. When the external NaCl was replaced by equipmolar concentrations of NaI, NaBr and NaNO₃, E_r was −33 ± 3.5 mV, −29.1 ± 5.2 mV and −18.4 ± 1.1 mV, respectively. 3 In physiological salt solution E_r of noradrenaline-evoked responses recorded with electrodes filled with 1m NaI or 1m NaNO₃ was + 16.3 + 3.9mV and +10.0 ± 7.6 mV, respectively. These results suggest that an increase in anion conductance contributes to the depolarization to noradrenaline. 4 Data from experiments with organic anions indicated that glutamate behaves as a less permeant anion but that benzenesulphonate blocks the anion conductance to unmask another conductance mechanism activated by noradrenaline. 5 When external NaCl was substituted by choline Cl and Tris Cl E_r was −21.3 ± 3.7 mV and −20.5 ± 2.8 mV, respectively. These results suggest that noradrenaline also activates a cation conductance mechanism in freshly dispersed rabbit portal vein cells. It is concluded that the depolarization to noradrenaline recorded with a microelectrode is produced by the simultaneous activation of an anion channel and a separate cation channel.