The behavior of the ouabain-insensitive sodium efflux in single barnacle muscle fibers toward the microinjection of aluminum

Abstract

Recent work with single muscle fibers from the barnacle Balanus nubilus has shown that the injection of Al into these fibers leads to inhibition of the resting Na efflux and that this involves both the ouabain-sensitive and the ouabain-insensitive components of the efflux. This work also showed that the injection of Al into ouabain-poisoned fibers oftern leads to a rise in the remaining Na efflux. This observation suggested the possibility that Al is able to stimulate the ouabain-insensitive Na by increasing myoplasmic free Ca 2+ and that trigger Ca 2+ reaches the myoplasm via voltage-dependent Ca 2+ channels. The results obtained are as follows: (i) The injection of AlCl 3 into fibers poisoned with ouabain produces a biphasic or monophasic effect on the remaining Na efflux. That is, stimulation is followed by inhibition, or there is only stimulation. (ii) This response is dose-dependent and is seen to take place following the injection of Al in a concentration as low as 0.01 m. (iii) Both Ga 3+ and Sc 3+ are able to mimick the effect of Al. (iv) Injection of EGTA following peak stimulation of the ouabain-insensitive Na efflux by injected AlCl 3 leads to reversal of this response. If, however, EGTA is injected long after the onset of peak stimulation and after ouabain reaches its maximum effect, it is found to be ineffective. (v) The magnitude of the stimulatory response of the ouabain-insensitive Na efflux is a sigmoidal function of external Ca 2+ and is almost completely abolished by verapamil, devapamil, and Cd 2+ but is unaffected by injecting Mg 2+ before or after AlCl 3. (vi) Whereas preinjection of Al reduces the response to ryanodine, external preapplication of ryanodine fails to alter the response to Al. The preinjection of deferoxamine (a potent chelator of Al) fails to stop the stimulatory response to Al injection from occurring. Taken together, these findings support the hypothesis that the stimulatory response elicited by Al injection is due to a fall in myoplasmic pCa resulting from activation of voltage-dependent Ca 2+ channels and that it involves the operation of the Na +Ca 2+ exchanger in the reverse mode.