REGULATION OF [CA2-MUSCLE BY CA2+-ATPASE AND NA+(](I) IN CANINE AIRWAY SMOOTH)CA2+ EXCHANGE MECHANISMS/

We investigated Ca2+ handling in airway smooth muscle (SM) using fura 2 fluorescence, ion currents, and contractions as indexes of intracell ular Ca2+ concentration ([Ca2+](i)). Carbachol evoked a transient elev ation of [Ca2+](i), the magnitude of which was smaller and the rate of decay faster at 37 degrees C, indicating that some temperature-sensit ive mechanism contributed to recovery Removal of external Na+ had no e ffect on agonist-evoked Ca2+ transients or contractions or on spontane ous Ca2+-dependent K+ currents. Cyclopiazonic acid, a selective inhibi tor of the sarcoplasmic reticulum (SR) Ca2+-ATPase, evoked a transient elevation of [Ca2+](i) and contraction, markedly slowed recovery of t he cholinergic Ca2+ transient, and depleted the SR. Sodium vanadate ev oked a sustained elevation of [Ca2+](i) and markedly slowed the decay of the cholinergic Ca2+ transient. We conclude that, in canine airway SM, 1) Na+/Ca2+ exchange makes at best only minor contribution to Ca2 homeostasis, 2) the SR Ca2+-ATPase compensates for spontaneous and ag onist-triggered release of Ca2+, and 3) [Ca2+](i) homeostasis involves some other extrusion pathway, likely the plasmalemmal Ca2+-ATPase.