Abstract
ATP is released from many cell types exposed to hypo-osmotic shock and is involved in RVD (regulatory volume decrease). Purinergic signalling events have been extensively investigated in mammals, but not in marine teleosteans. The effect of hypo-osmotic shock on ATP release was examined in isolated hepatocytes from turbot (Scophthalmus maximus), a marine flatfish. Hypo-osmotic stress (240 mOsm x kg(-1)) induced a significant increase in ATP efflux, and was inhibited by a potential CFTR (cystic fibrosis transmembrane conductance regulator) inhibitor, glibenclamide, but not by the MDR1 (multidrug resistance 1) P-glycoprotein inhibitor, verapamil. ATP efflux could be a cAMP-dependent process, as IBMX (isobutylmethylxanthine) and forskolin triggered the process under iso-osmotic conditions. Protein kinases, including protein kinase C, could also be involved, as staurosporine and chelerythrine inhibited the mechanism. Calcium could contribute to ATP efflux as ionomycin, a calcium ionophore, elicited a rapid release under iso-osmotic conditions, and chelation using EGTA abolished ATP release under hypo-osmotic conditions. RVD was partially abolished by apyrase, an ATP scavenger, and suramin, a purinoceptor antagonist. Moreover, hypo-...Continue Reading
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