Expression of KCa2.x and KCa3.1 channels in vascular smooth muscle cells from mouse portal vein

Abstract

Calcium‐activated K+ channels are key regulators of smooth muscle membrane potential, and therefore are essential to smooth muscle function. Small and intermediate conductance Ca2+‐activated K+ channels (KCa2.x and KCa3.1) have been reported in vascular myocytes only during proliferation. Portal vein is an atypical blood vessel as it shows action potentials (AP). As KCa2.x channels have been shown to be involved in the control of AP in different cell types, we investigated the presence of KCa2.x and KCa3.1 channels in vascular smooth muscle cells from mouse portal vein (mPV). PCR experiments showed the presence of mRNA for all KCa2.x and KCa3.1 channels in smooth muscle cells from mPV. In Patch clamp experiments, freshly isolated myocytes were dialyzed with a pipette solution containing 1 μM free Ca2+ to stimulate KCa channels. To minimize the contribution of BKCa channels, paxilline (10 μM) was added in the pipette as well as in the superfusion solution. Exposure of myocytes to TRAM‐34 (10 μM), an inhibitor of KCa3.1 channels, induced a decrease of ≈ 65% in membrane currents. However, Apamin (300 nM), a KCa2.x channels blocker, had little if any effect on membrane currents. These data suggest that KCa2.x and KCa3.1 channels are expressed in mPV and may play an important role in the control of membrane potential. This study is financially supported by FRSQ and the Fondation de l'Institut de Cardiologie de Montréal.