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

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 (Er) 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, Er was -33 +/- 3.5 mV, -29.1 +/- 5.2 mV and -18.4 +/- 1.1 mV, respectively. 3. In physiological salt solution Er of noradrenaline-evoked responses recorded with electrodes filled with 1 M NaI or 1 M NaNO3 was +16.3 +/- 3.9 mV 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 Er 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.