Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Abstract

1. The hypothesis that inward rectifier K+ channels are involved in the vasodilatation of small coronary and cerebral arteries (100-200 ,um diameter) in response to elevated [K+]. was tested. The diameters and membrane potentials of pressurized arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+]o from 6 to 16 mm caused the membrane potential of pressurized (60 mmHg) arteries to hyperpolarize by 12-14 mV. Extracellular Ba2P (Ba20+) blocked K+-induced membrane potential hyperpolarizations at concentrations (IC50, 6 uM) that block inward rectifier K+ currents in smooth muscle cells isolated from these arteries. 5. These findings suggest that K+ dilates small rat coronary and cerebral arteries through activation of inward rectifier K+ channels. Furthermore, these results support the hypothesis that inward rectifier K+ channels may be involved in metabolic regulation of coronary and cerebral blood flow in response to changes in [K+]0.

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

“…Although the polarity of the vascular response is inverted after SAH, both neurally evoked dilation (control) and constriction (SAH) involve the same mechanistic elements: increased endfoot Ca 2+ and K + efflux via endfoot BK channels. These responses reflect the dual vasodilator/vasoconstrictor potential of increased [K + ] o (21,38). Further, our present work indicates that SAH increases the amplitude of spontaneous Ca 2+ oscillations in astrocyte endfeet, leading to enhanced BK channel activity and elevated basal [K + ] o within the perivascular microdomain of brain cortex.…”

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).…”

“…Since their initial identification in rat cerebral and coronary artery (Edwards et al, 1988;Quayle et al, 1993;Knot et al, 1996), patch-clamp studies have reported strongly rectifying inward currents in isolated lung endothelial and bronchial smooth muscle cells (Voets et al, 1996;Kamouchi et al, 1997;Snetkov & Ward, 1999;Michelakis et al, 2001;Hogg et al, 2002;Oonuma et al, 2002;Shimoda et al, 2002).…”

An evaluation of potassium ions as endothelium‐derived hyperpolarizing factor in porcine coronary arteries

“…EDHF could be either the resultant of an electrotonic conduction of the endothelial cell hyperpolarization to the neighbouring smooth muscle cells or it could be potassium ions released by the endothelial cells during their hyperpolarizations (Chaytor et al, 1998;Edwards et al, 1998;Dora et al, 1999;Yamamoto et al, 1999). Depending upon the tissue, potassium ions would hyperpolarize the smooth muscle cells either by gating inward recti®ed potassium channels or by activating the sodium-potassium adenosine triphosphatase (Na + -K + ATPase), or both (Knot et al, 1996;Edwards et al, 1998;Prior et al, 1998).…”