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      Multiple Mechanisms of Activating Ca 2+ Entry in Freshly Isolated Rabbit Aortic Endothelial Cells


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          In Fura-2-loaded, freshly isolated rabbit aortic endothelial cells the Ca<sup>2+</sup> entry pathway was investigated using the Mn<sup>2+</sup>-quenching technique. Acetylcholine (ACh) interaction with muscarinic receptors activated Mn<sup>2+</sup> influx through the plasma membrane. Sarcoplasmic-endoplasmic reticulum Ca<sup>2+</sup> ATPase blockers such as cyclopiazonic acid (CPA), thapsigargin and BHQ, which block the endoplasmic reticulum Ca<sup>2+</sup> pump and do not interact with receptors, also activated Mn<sup>2+</sup> influx. Mn<sup>2+</sup> influx activated by either ACh or CPA was blocked by the following agents: SKF96365, a receptor-operated Ca<sup>2+</sup> channel (ROC) blocker; NCDC, a PLC and ROC blocker, and genistein, a tyrosine kinase inhibitor. D600, the L-type Ca<sup>2+</sup> channel blocker, had no significant effect on Mn<sup>2+</sup> influx. Caffeine blocked the ACh-induced Ca<sup>2+</sup> release but had no effect on the ACh-induced Mn<sup>2+</sup> influx. Similarly dantrolene, which blocked intracellular Ca<sup>2+</sup> release induced by ACh, did not affect the ACh-activated Mn<sup>2+</sup> influx. These data suggest that ACh can activate Ca<sup>2+</sup> influx without depletion of the ACh-sensitive intracellular Ca<sup>2+</sup> store. It is concluded (1) that in freshly isolated endothelial cells depletion of the intracellular Ca<sup>2+</sup> store is not necessary for ACh-activated Ca<sup>2+</sup> influx, and (2) that receptor activation and intracellular Ca<sup>2+</sup> store depletion may activate the same Ca<sup>2+</sup> entry pathway through parallel mechanisms.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          24 September 2008
          : 34
          : 3
          : 196-207
          Department of Pharmacology and Therapeutics, The University of British Columbia, Vancouver, Canada
          159223 J Vasc Res 1997;34:196–207
          © 1997 S. Karger AG, Basel

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          Page count
          Pages: 12


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