Modulation of calcium movements by urocortin II in endothelial cells

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Elena GrossiniGiovanni Vacca

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 ...Continue Reading

Citations

Jan 26, 2013·Journal of Molecular Endocrinology·E GrossiniG Vacca
Apr 30, 2016·Journal of Pharmacology & Pharmacotherapeutics·Elena GrossiniPatrizia Zeppegno
Mar 10, 2015·Drug Discovery Today·Rui AdãoCarmen Brás-Silva
Sep 13, 2019·Cardiovascular Drugs and Therapy·Cláudia Monteiro-PintoCarmen Brás-Silva

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