Ionic mechanisms involved in the strontium-induced spike and plateau in the smooth muscle of rat portal vein.

The action of Sr on the smooth muscle of rat portal vein was studied electrophysiologically using micro-electrodes. By replacing Ca with Sr (2.5 mM), the spontaneous membrane activity was altered and spikes were followed by a long lasting plateau potential. The mechanisms which generated the spike and the plateau in the Sr-induced activity were elucidated. As the concentration of Sr was increased, the peak potential and the maximum rates of rise and fall of the initial spike in each discharge increased. The peak potential varied by 15.2 mV with a 10-fold change in [Sr]o. As there was a decrease in the membrane resistance during the plateau, an increase in the permeability of the membrane for Sr, Cl or Na could be responsible for generation of the plateau. The amplitude of the plateau decreased with increase in the concentration of Sr, remained unchanged in a low-Cl solution, but was diminished in a low-Na solution. Mn (1-2 mM) inhibited not only the spike but also the plateau. TEA (20 mM) shifted the plateau potential in a positive direction and the plateau became permanent. When inward currents were applied in the presence of TEA, spikes with large overshoots and small rates of fall were induced. These results indicate that Sr and K conductances of the membrane generate the spike and that slow-inactivating voltage-dependent Na conductance produces the plateau.