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P₂ receptor-mediated Ca²⁺ transients in rat cerebral artery smooth muscle cells

Department of Human Anatomy and Cell Biology, University of Liverpool, Liverpool L69 3GE, United Kingdom

Submitted 2 June 2003 ; accepted in final form 16 September 2003

Significant Ca²⁺ release was previously noted with the activation of L-type Ca²⁺ current in rat superior cerebral artery smooth muscle cells. Here we examined whether the P_2X current that is partly carried by Ca²⁺ also triggers Ca²⁺ release in this preparation. Application of P_2X agonists evoked membrane currents and concomitant Ca²⁺ transients in whole cell voltage-clamped single cells. The expected increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) was calculated from the time-integrated P_2X current by assuming Ca²⁺ is the only charge carrier. The measured increase in [Ca²⁺]_i was plotted as a function of the expected increase in [Ca²⁺]_i, and Ca²⁺-buffering power was obtained as a reciprocal of the linear fit to this relationship. Both ryanodine, a Ca²⁺-induced Ca²⁺-release inhibitor, and cADP ribose, a putative activator of Ca²⁺-induced Ca²⁺ release, had no significant effects on Ca²⁺-buffering power. These results suggest that Ca²⁺ influx through P_2X receptors does not trigger significant Ca²⁺ release. We then examined whether P_2X responses influence the subsequent P_2Y response. P_2Y responses were characterized by measuring the rate of [Ca²⁺]_i increase obtained as the slope of the linear regression to the rising phase of the Ca²⁺ transient. During simultaneous application of the P_2X and P_2Y agonist, the rate of [Ca²⁺]_i increase was facilitated or suppressed depending on the size of the P_2X receptor-mediated [Ca²⁺]_i increase. Membrane depolarization close to the Ca²⁺ equilibrium potential significantly promoted the rate of [Ca²⁺]_i increase. Our results suggest that the [Ca²⁺]_i increase and membrane depolarization caused by the P_2X current may regulate the subsequent P_2Y response.

P_2x receptors; P_2y receptors; voltage clamp; sarcoplasmic reticulum; inositol 1,4,5-trisphosphate

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