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Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655
In airway smooth muscle
cells (SMCs) from mouse lung slices, 
10 µM ATP induced
Ca2+ oscillations that were accompanied by airway
contraction. After ~1 min, the Ca2+ oscillations subsided
and the airway relaxed. By contrast, 0.5 µM adenosine
5'-O-(3-thiotriphosphate) (nonhydrolyzable) induced Ca2+ oscillations in the SMCs and an associated airway
contraction that persisted for >2 min. Adenosine
5'-O-(3-thiotriphosphate)-induced Ca2+
oscillations occurred in the absence of external Ca2+ but
were abolished by the phospholipase C inhibitor U-73122 and the
inositol 1,4,5-trisphosphate receptor inhibitor xestospongin. Adenosine, AMP, and 
,
-methylene ATP had no effect on airway caliber, and the magnitude of the contractile response induced by a
variety of nucleotides could be ranked in the following order: ATP = UTP > ADP. These results suggest that the SMC response to ATP
is impaired by ATP hydrolysis and mediated via P2Y2 or
P2Y4 receptors, activating phospholipase C to release
Ca2+ via the inositol 1,4,5-trisphosphate receptor. We
conclude that ATP can serve as a spasmogen of airway SMCs and that
Ca2+ oscillations in SMCs are required to sustain airway contraction.
calcium signaling; confocal microscopy; ATP hydrolysis
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