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Properties of a store-operated nonselective cation channel in airway smooth muscle

¹ Dept of Medicine, McMaster University, and ² Firestone Institute for Respiratory Health, St. Joseph's Healthcare, Hamilton, ON, Canada

CORRESPONDENCE: L. J. Janssen, St. Joseph's Hospital, room L314, 50 Charlton Avenue East, Hamilton, ON, Canada, L8N 4A6, Fax: 1 9055406510E-mail: janssenl{at}mcmaster.ca

Keywords: Airway smooth muscle, BAPTA-AM, capacitative calcium entry, nonselective cation channel, single channel properties

Received: April 9, 2008
Accepted June 26, 2008

Passive depletion of internal Ca²⁺ stores in airway smooth muscle (ASM) activates nonselective cation channels (NSCCs) that mediate capacitative Ca²⁺ entry. However, the single channel properties of these cation channels have yet to be resolved and their regulation by cytosolic Ca²⁺ levels ([Ca²⁺]_i) still remains unclear.

NSCC currents and changes in [Ca²⁺]_i during passive depletion of internal Ca²⁺ stores were monitored in isolated bovine tracheal myocytes.

Loading cells with 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetracetic acid acetyl methyl ester (BAPTA-AM) to reduce [Ca²⁺]_i and thereby deplete the store augmented a basal Gd³⁺- and La³⁺-sensitive, Ca²⁺-permeable NSCC current. This current mimics that which is evoked by store depletion using the sarcoplasmic reticulum Ca²⁺ pump inhibitor cyclopiazonic acid (which concurrently and transiently elevates [Ca²⁺]_i). Both interventions activated an 25-pS NSCC with properties identical to both spontaneous (basal) and BAPTA-AM-evoked single channel currents.

In summary, the present study provides novel evidence that a lanthanide-sensitive, 25-pS nonselective cation channel underlies both basal and store depletion-evoked membrane currents in airway smooth muscle and that this conductance likely contributes to the regulation of resting [Ca²⁺]_i and capacitative Ca²⁺ entry.