The activation by potassium of the sodium—calcium carrier of cardiac mitochondria

In 1976 it was reported that cardiac mitochondria contain a Na+--Ca2+ antiporter [ 11, and subsequent work has established that this carrier is present also in mitochondria of several other tissues [2][3][4].The properties of the antiporter indicate that it is quite distinct from the carrier (uniporter) that catalyzes Ca2+ influx [ 5,6] and that its natural role is to catalyze the efflux of Ca2+ from mitochondria [l-3,5].The simultaneous catalysis of Ca2+ flux by the uniporter and antiporter generates Ca2+ recycling across the inner membrane, and a steady state is attained when the activities of the two Ca2+ carriers are equal.[1,2,7,81.It has been proposed that the function of the cycle in cardiac mitochondria is the control of the intramitochondrial free [Ca"] in accordance with the regulatory requirements of certain dehydrogenases of the citric acid cycle [9,10].However, to evaluate the capacity of the cycle to control the transmembrane distribution of Ca2+, and in particular the intramitochondrial free [Ca"], it is clearly necessary to establish the factors that influence the activities of the uniporter and antiporter.This report presents evidence that the antiporter, but not the uniporter, is strongly activated by K+.Both the Nd-Ca2+ and Ca2+-Ca2+ exchange activities of the antiporter are affected.