Referenced in: none

Automatically associated channels: Slo1

Title: Modulation of calcium movements by urocortin II in endothelial cells.

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

Journal, date & volume: Cell. Physiol. Biochem., 2010 , 25, 221-32

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20110683

Abstract
In endothelial cells urocortin II has recently been found to activate nitric oxide synthase through cAMP-dependent and Ca(2+)-related pathway.The present study was therefore planned to determine the mechanisms of urocortin II effect on Ca(2+) movements.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.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.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.