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K IR channels function as electrical amplifiers in rat vascular smooth muscle
Author(s) -
Smith Pamela D.,
Brett Suzanne E.,
Luykenaar Kevin D.,
Sandow Shaun L.,
Marrelli Sean P.,
Vigmond Edward J.,
Welsh Donald G.
Publication year - 2008
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.145474
Subject(s) - conductance , vascular smooth muscle , cerebral arteries , electrophysiology , mesenteric arteries , hyperpolarization (physics) , electrical impedance myography , coronary arteries , chemistry , biophysics , artery , anatomy , medicine , smooth muscle , biology , vasodilation , physics , stereochemistry , nuclear magnetic resonance spectroscopy , condensed matter physics
Strong inward rectifying K + (K IR ) channels have been observed in vascular smooth muscle and can display negative slope conductance. In principle, this biophysical characteristic could enable K IR channels to ‘amplify’ responses initiated by other K + conductances. To test this, we have characterized the diversity of smooth muscle K IR properties in resistance arteries, confirmed the presence of negative slope conductance and then determined whether K IR inhibition alters the responsiveness of middle cerebral, coronary septal and third‐order mesenteric arteries to K + channel activators. Our initial characterization revealed that smooth muscle K IR channels were highly expressed in cerebral and coronary, but not mesenteric arteries. These channels comprised K IR 2.1 and 2.2 subunits and electrophysiological recordings demonstrated that they display negative slope conductance. Computational modelling predicted that a K IR ‐like current could amplify the hyperpolarization and dilatation initiated by a vascular K + conductance. This prediction was consistent with experimental observations which showed that 30 μ m Ba 2+ attenuated the ability of K + channel activators to dilate cerebral and coronary arteries. This attenuation was absent in mesenteric arteries where smooth muscle K IR channels were poorly expressed. In summary, smooth muscle K IR expression varies among resistance arteries and when channel are expressed, their negative slope conductance amplifies responses initiated by smooth muscle and endothelial K + conductances. These findings highlight the fact that the subtle biophysical properties of K IR have a substantive, albeit indirect, role in enabling agonists to alter the electrical state of a multilayered artery.