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Calcium Mobilization and Spontaneous Transient Outward Current Characteristics upon Agonist Activation of P2Y₂ Receptors in Smooth Muscle Cells

G. Lemon ^*, J. Brockhausen , G.-H. Li , W. G. Gibson ^* and M. R. Bennett 

^* The School of Mathematics and Statistics, University of Sydney, New South Wales, Australia; and The Neurobiology Laboratory, Department of Physiology, The Institute for Biomedical Research, University of Sydney, New South Wales, Australia

Correspondence: Address reprint requests to Professor Max Bennett, Neurobiology Laboratory, University of Sydney, N.S.W. 2006, Australia. E-mail: maxb{at}physiol.usyd.edu.au.

A quantitative model is provided that links the process of metabotropic receptor activation and sequestration to the generation of inositol 1,4,5-trisphosphate, the subsequent release of calcium from the central sarcoplasmic reticulum, and the consequent release of calcium from subsarcolemma sarcoplasmic reticulum that acts on large-conductance potassium channels to generate spontaneous transient outward currents (STOCs). This model is applied to the case of STOC generation in vascular A7r5 smooth muscle cells that have been transfected with a chimera of the P2Y₂ metabotropic receptor and green fluorescent protein (P2Y₂-GFP) and exposed to the P2Y₂ receptor agonist uridine 5'-triphosphate. The extent of P2Y₂-GFP sequestration from the membrane on exposure to uridine 5'-triphosphate, the ensuing changes in cytosolic calcium concentration, as well as the interval between STOCs that are subsequently generated, are used to determine parameter values in the model. With these values, the model gives a good quantitative prediction of the dynamic changes in STOC amplitude observed upon activation of metabotropic P2Y₂ receptors in the vascular smooth muscle cell line.

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