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Abstract

Although lanthanum ions (La+++) block calcium influx in cardiac cells, they may paradoxically accentuate the sodium-free contracture. We have therefore studied the effects of La+++ on the zero sodium response in chick embryonic myocardial cell aggregates. Zero sodium alone causes: (a) A maintained contracture; (b) Asynchronous localized contractions that are selectively inhibited by caffeine or ryanodine, and presumably reflect release of calcium from the sarcoplasmic reticulum; (c) A nonspecific conductance increase that is ascribable to calcium-activated ion channels. Addition of La+++ potentiates the sodium-free contracture, and causes similar potentiation of the localized contractions and the conductance increase. All three phenomena occur 5–10-fold faster in 1 mM La+++ than in sodium-free fluid alone. In contrast, when La+++ is combined with caffeine or ryanodine, the zero sodium response is suppressed. We conclude that the paradoxical effect of La+++ on the contracture is not due to calcium influx, but to enhancement, or disinhibition of intracellular calcium release. Relaxation of normal myocardium may involve control of spontaneous calcium release by lanthanum- and sodium-sensitive calcium transport across the surface membrane.