Palytoxin acidifies chick cardiac cells and activates the Na+/H+ antiporter.
The cardiotoxic action of palytoxin was investigated using embryonic chick ventricular cells. Under normal ionic conditions, palytoxin produced an intracellular acidification which is partially compensated for by the Na+/H+ antiporter thereby leading to an increased rate of ethylisopropylamiloride-sensitive 22Na+ uptake. Under depolarizing membrane conditions, palytoxin produced a cellular acidification, a cellular alkalinization or no change in intracellular pH depending on the value of the extracellular pH. We propose that palytoxin acidifies cardiac cells by opening preexisting H+ conducting pathways in the plasma membrane.
Frelin
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Institut de Pharmacologie Moléculaire et Cellulaire, UPR 411, CNRS, Valbonne, France.
Vigne
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Breittmayer
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JP
D000178:Acrylamides; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D002478:Cells, Cultured; D002642:Chick Embryo; D003064:Cnidarian Venoms / Q000494:pharmacology*; D006352:Heart Ventricles / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D009206:Myocardium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers; D000095702:Polyether Toxins
D000178:Acrylamides; D002352:Carrier Proteins; D003064:Cnidarian Venoms; D012964:Sodium; D017923:Sodium-Hydrogen Exchangers; C010272:palytoxin; D000095702:Polyether Toxins