Activation thresholds of Kv, BK and ClCa channels in smooth muscle cells in pial precapillary arterioles

We have previously shown expression of voltage-gated K+ channels (K-V) in smooth muscle of cerebral arterioles and suggested the channels function to oppose voltage-dependent Ca2+ entry. However, other studies indicate that large conductance Ca2+-activated K+ (BK) channels serve this function and chloride (Cl-) channels may have the opposite effect. In this study we compared the activation thresholds and absolute current amplitudes for K-V channels, BK channels and Cl- channels at physiological membrane potentials in intact precapillary arterioles from the rabbit cerebral circulation. Patch-clamp recordings were made to measure current and membrane potential, and a video scan line was used to detect external diameter. Two strategies to determine the basal current-voltage relationship of BK channels showed the channels contributed current only at voltages positive of -35 mV, even though voltage-dependent Ca2+-entry occurred. Ca2+-activated and niflumic acid-sensitive Cl- current was detected but, between -50 and -10 mV, both BK and Cl- channel currents were much smaller and contributed less to the membrane potential compared with K-V channel current. Furthermore, in the absence of an exogenous vasoconstrictor agent, block of K-V channels but not BK or Cl- channels caused constriction, although in the presence of endothelin-1 block of BK or K-V channels caused constriction. The data indicate K-V channels are the first inhibitory mechanism to activate when there is depolarisation in precapillary arteriolar smooth muscle cells of the cerebral circulation. Copyright (C) 2002 S. Karger AG, Basel.