Modulation of calcium movements by urocortin II in endothelial cells

Elena Grossini, Philippe Primo Caimmi, Claudio Molinari, David A.S.G. Mary, Francesca Uberti, Giovanni Vacca

Research output: Contribution to journalArticlepeer-review

Abstract

Background: In endothelial cells urocortin II has recently been found to activate nitric oxide synthase through cAMP-dependent and Ca 2+ - related pathway. Aim: The present study was therefore planned to determine the mechanisms of urocortin II effect on Ca 2+ movements. Methods. In Fura-2 loaded porcine aortic endothelial cells (PAE), the effects of urocortin II on [Ca 2+ ]c were analyzed and compared with those of various K + channels agonists/antagonists. Results: In Fura-2 loaded PAE, urocortin II promoted a transient increase of [Ca 2+ ]c mainly originating from an intracellular pool sensitive to thapsigargin and slightly from the extracellular space. In addition, urocortin II caused the hyperpolarization of plasma membrane through the opening of K + channels, which contributed to the increased [Ca 2+ ]c. These effects were abolished by the corticotropin releasing factor receptors (CRFR2) blocker, the adenylyl cyclase and Ca 2+ -calmodulin-kinase (CaMKII) inhibitors and by blockers of K + channels. In addition, in PAE cultured in Na + -free medium or loaded with the plasma-membrane Ca 2+ pump inhibitor the urocortin II-evoked Ca 2+ transient was slower. Conclusion: The results obtained show that urocortin II affects intracellular Ca 2+ homeostasis in PAE by both promoting a discharge of intracellular pool and by interfering with the operation of store-dependent channels through CRFR2-cAMP-CaMKII related signalling and K + channels opening.

Original languageEnglish
Pages (from-to)221-232
Number of pages12
JournalCellular Physiology and Biochemistry
Volume25
Issue number2-3
DOIs
Publication statusPublished - 2010

Keywords

  • Calcium movements
  • Endothelial cells
  • Potassium channels
  • Urocortin II

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