Inward rectifying potassium channels facilitate cell-to-cell communication in hamster retractor muscle feed arteries.
This study examined whether inward rectifying K+ (KIR) channels facilitate cell-to-cell communication along skeletal muscle resistance arteries. With the use of feed arteries from the hamster retractor muscle, experiments examined whether KIR channels were functionally expressed and whether channel blockade attenuated the conduction of acetylcholine-induced vasodilation, an index of cell-to-cell communication. Consistent with KIR channel expression, this study observed the following: 1) a sustained Ba2+-sensitive, K+-induced dilation in preconstricted arteries; 2) a Ba2+-sensitive inwardly rectifying K+ current in arterial smooth muscle cells; and 3) KIR2.1 and KIR2.2 expression in the smooth muscle layer of these arteries. It was subsequently shown that the discrete application of acetylcholine elicits a vasodilation that conducts with limited decay along the feed artery wall. In the presence of 100 microM Ba2+, the local and conducted response to acetylcholine was attenuated, a finding consistent with a role for KIR in facilitating cell-to-cell communication. A computational model of vascular communication accurately predicted these observations. Control experiments revealed that in contrast to Ba2+, ATP-sensitive- and large-conductance Ca2+ activated-K+ channel inhibitors had no effect on the local or conducted vasodilatory response to acetylcholine. We conclude that smooth muscle KIR channels play a key role in facilitating cell-to-cell communication along skeletal muscle resistance arteries. We attribute this facilitation to the intrinsic property of negative slope conductance, a biophysical feature common to KIR2.1- and 2.2-containing channels, which enables them to increase their activity as a cell hyperpolarizes.
Jantzi
Micaela C
MC
Smooth Muscle Research Group and the Department of Physiology and Biophysics, HM-86, Heritage Medical Research Bldg., 3330 Hospital Dr., NW, University of Calgary, Alberta, Canada, T2N-4N1.
Brett
Suzanne E
SE
Jackson
William F
WF
Corteling
Randolph
R
Vigmond
Edward J
EJ
Welsh
Donald G
DG
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001158:Arteries / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D001464:Barium / Q000494:pharmacology; D002450:Cell Communication / Q000502:physiology*; D003198:Computer Simulation; D006224:Cricetinae; D005786:Gene Expression Regulation / Q000502:physiology; D005905:Glyburide / Q000494:pharmacology; D008297:Male; D008647:Mesocricetus; D018482:Muscle, Skeletal / Q000098:blood supply*; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
D000889:Anti-Arrhythmia Agents; C489461:Kir2.1 channel; C489463:Kir2.2 channel; D024661:Potassium Channels, Inwardly Rectifying; D001464:Barium; D000109:Acetylcholine; D005905:Glyburide