Inward rectifier K+ currents in smooth muscle cells from rat coronary arteries: block by Mg2+, Ca2+, and Ba2+

Abstract

Inward rectifier K+ channels have been implicated in the control of membrane potential and external K(+)-induced dilations of small coronary arteries. To identify and characterize inward rectifier K+ currents in coronary artery smooth muscle, whole cell K+ currents in smooth muscle cells enzymatically isolated from rat coronary (septal) arteries (diameters, 100-150 microns) were measured in the conventional and perforated configurations of the patch-clamp technique. Ba(2+)-sensitive, whole cell K+ current-voltage relationships exhibited inward rectification. Blockers of Ca(2+)-activated K+ channels (1 mM tetraethylammonium ion), ATP-sensitive K+ channels (10 microM glibenclamide), and voltage-dependent K+ channels (1 mM 4-aminopyridine) in smooth muscle did not affect inward rectifier K+ currents. The nonselective K+ channel inhibitor phencyclidine (100 microM) reduced inward rectifier K+ currents by approximately 50%. External Ba2+ reduced inward currents, with membrane potential hyperpolarization increasing inhibition. The half-inhibition constant for Ba2+ was 2.1 microM at -60 mV, decreasing e-fold for a 25-mV hyperpolarization. External Cs+ also blocked inward rectifier K+ currents, with the half-inhibition constant for Cs+ of 2.9 mM at -60 mV. External Ca2+ and Mg2+ reduced inward rectifier K+ currents. At -60 mV, Ca2+ and Mg2+ (1 mM) reduced inward currents by 33 and 21%, respectively. Inward rectification was not affected by dialysis of the cell's interior with a nominally Ca(2+)- and Mg(2+)-free solution. These findings indicate that inward rectifier K+ channels exist in coronary artery smooth muscle and that Ba2+ may be a useful probe for the functional role of inward rectifier K+ channels in coronary arteries.

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

“…However, at least one mechanism would be a plausible reason. As high K + induced an increase in K ir conductance (Jiang et al, 2001;Robertson et al, 1996), which was indicated by an initial transient large hyperpolarization followed by a small sustained hyperpolarization in high V m cells (Fig. 7C, also (Jiang et al, 2001), the increased K ir conductance should exert a shunting effect on the ACh-induced current, causing a reduction of the depolarization.…”

Kir2.1 encodes the inward rectifier potassium channel in rat arterial smooth muscle cells

“…The endothelium was removed on a portion of the artery samples by inverting the artery and scraping the lumenal surface with a glass slide. Vascular smooth muscle cells were isolated by a procedure previously described (Robertson et al 1996). Briefly, intact arteries were placed into the above-mentioned extracellular solution which included 1 mg ml¢ papain, 1 mg ml¢ bovine serum albumin (BSA), and 1 mg ml¢ dithioerythritol, and incubated for various time periods (20 min for coronary arteries; 30 min for basilar arteries; 35 min for mesenteric arteries) at 37°C.…”

“…Previous studies have demonstrated that strong, inwardly rectifying K¤ currents in native vascular smooth muscle cells are sensitive to extracellular K¤ and low (ìÒ) concentrations of Ba¥ (Quayle et al 1993;Robertson et al 1996). It has previously been shown that a change in external K¤ had a number of effects on Kir currents: (1) rectification shifted with EK; (2) Erev for the current was a function of the EK; and (3) inward conductance increased with external K¤ concentration.…”

Functional Expression of Inward Rectifier Potassium Channels in Cultured Human Pulmonary Smooth Muscle Cells: Evidence for a Major Role of Kir2.4 Subunits

“…Regardless of their origin within the cardiovascular system, K IR currents recorded to date are potently blocked by micromolar external Ba 2+ ions in a manner that is steeply voltage and time-dependent (Quayle et al, 1993;Robertson et al, 1996;Bradley et al, 1999;Snetkov & Ward, 1999;Sakai et al, 2002;Oonuma et al, 2002).…”