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      Calcium-release-activated calcium influx in endothelium.

      Journal of Vascular Research

      Animals, metabolism, Tyrosine, Swine, pharmacology, Substance P, drug effects, Potassium Channels, Phosphorylation, Nitric Oxide, Male, In Vitro Techniques, Female, cytology, Endothelium, Vascular, Coronary Vessels, Calcium, Arterioles

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          Abstract

          Signaling pathways activated by the tachykinin substance P (SP) were investigated in pig coronary artery endothelial cells (PCAECs). Single cells were obtained after enzymatic digestion of coronary arteries. Intracellular Ca2+ ([Ca2+]i) was measured from fura-2 fluorescence while membrane potential or ionic current was measured using patch-clamp techniques. In physiological saline solution, SP induced hyperpolarizations or outward currents which coincided with biphasic [Ca2+]i increases representing store release of Ca2+ and Ca2+ influx. Single channel recording protocols showed that both sources of Ca2+ activated a small conductance K+ channel, resulting in cell hyperpolarization. When outward currents were blocked by d-tubocurare, Cs+, or BAPTA, an inward current was unmasked. Ion substitution protocols showed that the SP-induced inward current was (1) carried by a mixture of Ca2+ and Na+, (2) blocked by La3+, and (3) inactivated by high extracellular [Ca2+]. Tyrosine kinase inhibitors also blocked the inward current. The same current was activated by bath application of BHQ, an inhibitor of the endoplasmic reticulum Ca2+ ATPase, or by cell dialysis with IP3. These results suggest that the plateau phase of the agonist-activated [Ca2+]i increase in PCAECs reflects Ca2+ entry through a depletion-activated Ca2+ channel. The characteristics of this channel are compared to those of Ca2+ channels found in other nonexcitable cells.

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