INTRINSIC GATING OF INWARD RECTIFIER IN BOVINE PULMONARY-ARTERY ENDOTHELIAL-CELLS IN THE PRESENCE OR ABSENCE OF INTERNAL MG-2+

Inward rectifier (IR) currents were studied in bovine pulmonary artery endothelial cells in the whole-cell configuration of the patch-clamp technique with extracellular K+ concentrations, [K+]0, ranging from 4.5 to 160 mM. Whether the concentration of free Mg2+ in the intraceUular solution, [Mg2+]i, was 1.9 mM or nominally 0, the IR exhibited voltage- and time-dependent gating. The IR conductance was activated by hyperpolarization and deactivated by depolarization. Small steady-state outward IR currents were present up to ~40 mV more positive than the K+ reversal potential, EK, regardless of [Mg2+]i. Modeled as a first-order C⇄O gating process, both the opening rate, α, and the closing rate,β, were exponentially dependent on voltage, withβ more steeply voltage dependent, changing e-fold for 9 mV compared with 18 mV for an e-fold change in α. Over all [K+]0 studied, the voltage dependence of α and β shifted along with EK, as is characteristic of IR channels in other cells. The steady-state voltage dependence of the gating process was well described by a Boltzmann function. The half-activation potential was on average ~7 mV negative to the observed reversal potential in all [K+]0 regardless of [Mg2+]i. The activation curve was somewhat steeper when Mg-free pipette solutions were used (slope factor, 4.3 mV) than when pipettes contained 1.9 mM Mg2+ (5.2 mV). The simplest interpretation of these data is that IR channels in bovine pulmonary artery endothelial cells have an intrinsic gating mechanism that is not due to Mg block. © 1990, Rockefeller University Press., All rights reserved.