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Palytoxin acidifies chick cardiac cells and activates the Na + /H + antiporter
Author(s) -
Frelin Christian,
Vigne Paul,
Breittmayer Jean-Philippe
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80765-b
Subject(s) - palytoxin , antiporter , intracellular , extracellular , biophysics , intracellular ph , depolarization , amiloride , ion transporter , membrane , membrane potential , biology , biochemistry , chemistry , sodium , toxin , organic chemistry
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 ethylisopropylami‐loride‐sensitive 22 Na + 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.