title: Palytoxin acidifies chick cardiac cells and activates the Na+/H+ antiporter.
abstract: 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.
authors.affiliation: Institut de Pharmacologie Moléculaire et Cellulaire, UPR 411, CNRS, Valbonne, France.
authors.forename: C
authors.initials: C
authors.lastname: Frelin
authors.forename: P
authors.initials: P
authors.lastname: Vigne
authors.forename: J P
authors.initials: JP
authors.lastname: Breittmayer
mesh_terms: 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
chemical_list: D000178:Acrylamides; D002352:Carrier Proteins; D003064:Cnidarian Venoms; D012964:Sodium; D017923:Sodium-Hydrogen Exchangers; C010272:palytoxin; D000095702:Polyether Toxins