Abstract
Valinomycin in the presence of potassium is a potent uncoupler of corn (Zea mays L.) mitochondria, eliminating respiratory control. Valinomycin produces higher steady state potassium phosphate swelling which can be reversed to give active shrinkage if mersalyl is added to block the Pi(-)/OH(-) antiporter. Respiration declines concurrently. Uncouplers accelerate the shrinkage and restore the respiration. The same results can be obtained with sodium phosphate if gramicidin D is substituted as ionophore.It is concluded that valinomycin uncoupling is the result of cyclic salt transport, with influx pumping of potassium phosphate via the Pi(-)/OH(-) antiporter and efflux pumping via a K(+)/H(+) antiporter. The result is a higher level of steady state swelling, rapid turnover of the proton gradient, and uncoupled respiration rates. The level of steady state swelling can be manipulated by varying the valinomycin or K(+) concentrations, with high concentrations favoring activation of the efflux pump.A mosaic membrane model with high resistance for proton and monovalent cation penetration to the cation(+)/H(+) antiporter is used to explain the results.