Abstract
Urocortin (UCN) II, a newly isolated corticotropinreleasing-factor (CRF) related peptide, has beenfound to have potent cardiovascular protective effects.To investigate the mechanisms of its vascularprotective effects, we exposed mesenteric arterialsmooth muscle cells (MASMC) from spontaneouslyhypertensive rats (SHR) to UCN II to observe thechange in cell apoptosis using TUNEL assay andmeasured intracellular calcium concentration ([Ca2+]i)using confocal laser scanning microscope. In addition,effects of UCN II on L-type calcium currents (ICa,L) werealso measured using whole-cell patch clamp. Ourresults showed that UCN II concentration-dependently,but time-independently inhibited cell apoptosis.Astressin 2B, a special CRF 2 receptor antagonist,had no influence on this inhibition. Hypoxia or BayK8644, the L-type calcium channel activator, inducedthe apoptosis of MASMC from SHR. Pretreatment ofthe cells with UCN II diminished the effects of hypoxiaor Bay K8644. UCN II was also observed to reduce[Ca2+]i increase induced by KCl or Bay K8644. UCN IIconcentration-dependently inhibited ICa,L, which wasnot affected by astressin 2B. It did not affect theactivation of ICa,L, but markedly shifted the inactivationcurve to the left. In conclusion, UCN II inhibits theapoptosis of MASMC from SHR via inhibiting L-typecalcium channels.
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