Abstract
The rate, extent, and efficiency of the energy-dependent contraction of heart mitochondria swollen in Na+ or K+ nitrate are all strongly activated by nigericin, an antibiotic which is known to support cation/H+ exchange in natural and model membranes. In the absence of nigericin, the cation selectivity sequence of energy-dependent contraction (Na+>Li+>K+>choline+) is identical to that of passive swelling in acetate salts, a reaction which is presumed to be dependent on an endogenous cation/H+ exchanger. These results strongly favor an osmotic mechanism for energy-dependent contraction which depends on electrogenic H+ ejection, H+/cation exchange, and electrophoretic anion efflux.
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