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1 Department of Medicine, McMaster University, Hamilton, ON, Canada
* To whom correspondence should be addressed. E-mail: janssenl{at}mcmaster.ca.
Capacitative Ca2+ entry has been examined in several tissues and, in some, appears to be mediated by non-selective cation channels collectively referred to as "storeoperated" cation channels, however relatively little is known about the electrophysiological properties of these channels in airway smooth muscle. Consequently we examined the electrophysiological characteristics and changes in [Ca2+]i associated with a cyclopiazonic acid (CPA)-evoked current in porcine and bovine airway smooth muscle using patch clamp and Ca2+-fluorescence techniques. In bovine tracheal myocytes, CPA induced an elevation of [Ca2+]i that was dependent upon extracellular Ca2+ and was insensitive to nifedipine (an L-type voltage-gated Ca2+ channel inhibitor). Using patch-clamp techniques, and conditions that block both K+ and Cl- currents, we found that CPA rapidly activated a membrane conductance (ICPA) in porcine and bovine tracheal myocytes which exhibits a linear current-voltage relationship with a reversal potential (Erev) around ~0 mV. Replacement of extracellular Na+ resulted in a marked reduction of ICPA at physiological membrane potentials (i.e., -60 mV) that was accompanied by a shift in the reversal potential for ICPA towards more negative membrane potentials. In addition, ICPA was markedly inhibited by 10 µM Gd3+ and La3+ but was largely insensitive to 1µM nifedipine. We conclude that CPA induces capacitative Ca2+ entry in porcine and bovine tracheal smooth muscle via a Gd3+- and La3+-sensitive, non-selective cation conductance.
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