The properties and distribution of inward rectifier potassium currents in pig coronary arterial smooth muscle.

Abstract

1. Whole-cell potassium currents were studied in single smooth muscle cells enzymatically isolated from pig coronary arteries. 2. In cells isolated from small diameter branches of the left anterior descending coronary artery (LAD), an inward rectifier potassium current (IK(IR)) was identified, which was inhibited by extracellular barium ions, suggesting the presence of inward rectifier potassium (KIR) channels.3. The conductance for IK(IR) measured in 6, 12, 60 and 140 mm extracellular potassium was a function of membrane potential and the extracellular potassium concentration. 4. On hyperpolarization, IK(IR) activated along an exponential time course with a time constant that was voltage dependent. 5. Inward rectifier current was compared in cells isolated from coronary vessels taken from different points along the vascular tree. Current density was greater in cells isolated from small diameter coronary arteries; at -140 mV it was -20f5 + 4f4 pA pF-' (n = 23) in 4th order branches of the LAD, but -0 8 + 0 2 pA pF-' (n = 11) in the LAD itself.6. In contrast to 'K(IR)' there was little effect of arterial diameter on the density of voltagedependent potassium current; densities at +30 mV were 12 8 + 1 3 pA pF-' (n = 19) in 4th order branches and 17 4 + 3 1 pA pF-' (n = 11) in the LAD.7. We conclude that KIR channels are present in pig coronary arteries, and that they are expressed at a higher density in small diameter arteries. The presence of an enhanced IK(IR) may have functional consequences for the regulation of cell membrane potential and tone in small coronary arteries.

Potassium does not mimic EDHF in rat mesenteric arteries

“…It has previously been shown in the coronary circulation, that the density of K ir channels is inversely related to arterial size. The consequence of this is that mechanisms dependent upon the activation of K ir become increasingly important in smaller arteries (Quayle et al, 1993(Quayle et al, , 1996. This would be consistent with the hypothesis that EDHF becomes progressively more important as arterial diameter decreases (Shimokawa et al, 1996).…”

“…Even if raising [K + ] o failed to dilate, 10 mM ACh in the presence of high [K + ] o was still able to dilate to the passive diameter (n=7) ( Figure 1A and B). In rat coronary artery K ir is present in small but not large rat coronary arteries (Quayle et al, 1996). However, the ability of raised [K + ] o to produce dilatation in rat mesenteric arteries was not correlated with the artery diameter for the range tested (200 ± 400 mm) ( Figure 1C ] o in the superfusate failed to produce dilatation, then it also failed to produce dilatation when co-applied lumenally (n=3).…”

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

“…K IR channels have been suggested to play an important role in maintaining the resting membrane potential and involved in the K + -induced hyperpolarization of vascular smooth muscle (Edwards et al, 1988;Knot et al, 1996;Quayle et al, 1996;Quayle et al, 1997). In some vessels, K IR channels are the target for endothelium-derived hyperpolarising factor (EDHF) where K + , liberated via endothelial Ca 2+ -sensitive K + channels, is thought to activate K IR channels within the smooth muscle layer (Edwards & Weston, 2004).…”

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

“…This shift was probably due to an inhibition of K ir current since it is known that K ir conductance is extracellular K + -dependent and also that 100 μM Ba 2+ mimics the action of zero K + (Jiang et al, 2001;Quayle et al, 1996). The high K + (20 mM) solution also caused a 20 -30 mV persistent depolarization in such cells, owing to the change of E K value (Jiang et al, 2001).…”