Pharmacological evaluation of early afterdepolarisations induced by sea anemone toxin (ATXII) in dog heart

Abstract

ATXII induced early after depolarisations are due to the effects of ATXII on Na+ entry, probably via a slowly inactivated Na+ channel population. Calcium entry through the sarcolemmal Ca2+ channels and cyclic Ca2+ release from the sarcoplasmic reticulum are not required for the genesis of early afterdepolarisations in this model.