Membrane ionic mechanisms activated by noradrenaline in cells isolated from the rabbit portal vein.

Abstract

Membrane currents were recorded in cells freshly dispersed from the rabbit portal vein with patch pipette techniques in the whole-cell configuration of recording. In potassium-containing solutions at a holding potential of -50 mV noradrenaline usually evoked an inward current and enhanced greatly the outward current evoked by depolarizing voltage steps. The ionic mechanism of the inward current was investigated in potassium-free solutions in which the inward current elicited by noradrenaline was produced by an increase in membrane conductance. In the first series of experiments NaCl was the main salt in the patch pipette solution (representing the intracellular milieu) and the ionic composition of the bathing solution was altered. In these conditions the reversal potential of the noradrenaline-induced current was close to the chloride equilibrium potential (ECl). When sodium glutamate was the major salt in the pipette solution the reversal potential of the noradrenaline-evoked current was influenced by the cation rather than the anion gradient. With 89 mM-BaCl2 in the external solution (and sodium glutamate in the pipette) noradrenaline produced a membrane current with a reversal potential which was much more positive than ECl or ENa. These results indicate that noradrenaline opens a chloride-selective channel and a cation channel which is permeable to monovalent and divalent cations. Bath application of 10 mM-caffeine evoked a membrane current with a reversal potential close to ECl with either NaCl or sodium glutamate in the pipette. This is interpreted to mean that the increase in membrane chloride conductance can occur as a consequence of a rise in intracellular calcium concentration. It is less evident that the cation channel is calcium activated.