Abstract
The effects of manganese chloride were studied on Na-Ca exchange fluxes from intact squid axons. Ca uptakes and Ca o-dependent sodium efflux were inhibited half-maximally by 3–7 mM MnCl 2. Mn inhibition appears less during Na o-Ca i exchange (half-maximal inhibition; 30 mM) than that during Ca o-Na i exchange, even when both fluxes were activated with 100 mM Na. The effects of changes in [Ca i 2+], effected by Ca-EGTA injection or inhibition of mitochondrial Ca uptake by ruthenium red, were examined on the reverse (Ca o-Na i) exchange mode. Ca-EGTA mixtures, designed to raise [Ca i 2+] above 2 μM, inhibited Ca o-Na i exchange fluxes. Ruthenium red inhibited mitochondrial Ca buffering to effect increases in Ca i in the absence of Ca chelators; it activated Na o-Ca i exchange fluxes but had little effect on Ca o-Na i exchange despite similar reported K m for Ca i. The results reflect the difficulty in demonstrating the stimulatory effect of [Ca i 2+] on Ca o-Na i exchange fluxes in intact axons.
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