The na+-h+ antiport in renal mitochondria.
Sastrasinh, Malinee, Patricia Young, Edward J. Cragoe, Jr, Sithiporn
Sastrasinh.
DVA Medical Center, East Orange 07018-1095; University of Medicine and
Dentistry-New Jersey Medical School, Newark, New Jersey 07103-2714
APStracts 2:0036C, 1995.
In isolated renal mitochondria Na+ and Li+ stimulated H+ efflux from the
mitochondrial matrix. In submitochondrial particles (SMP) Na+ flux was also
coupled to H+ transport in the opposite direction. The overshoot of Na+
uptake in SMP with an outwardly direct ed H+ gradient indicated that downhill
efflux of H+ through the mitochondrial membrane induced uphill transport of
Na+. Similar to the Na+-H+ antiport in other types of mito chondria, the
antiport in renal mitochondria was more sensitive to amiloride derivatives
than to amiloride itself. Benzamil and EIPA, but not amiloride, inhibited the
antiport with fifty percent inhibition of 10-4 M for both benzamil in
mitochondria and EIPA in SMP. The Na+-H+ antiport in renal mitochondria had
simple saturation kinetics for outside Na+ (Km = 3.27 +/- 0.63 mM; Vmax =
0.022 +/- 0.002 pH unit.s-1) and Li+ (Km = 3.62 +/- 0.75 mM; Vmax = 0.022 +/-
0.002 pH unit.s-1). NH4Cl and NH4 acetate stimulated Na+ efflux and inhibited
Na+ uptake in SMP. Comparable results with NH4 acetate and chloride sug gested
that NH4+ modified Na+ transport through its direct interaction with the Na+
-H+ antiport, rather than through the alkalinization of intra-SMP space from
non-ionic diffusion of NH3. These results suggested that the Na+-H+ antiport
may be a factor in the exit of NH4+ from renal mitochondria.
Received 2 November 1993; accepted in final form 18 November 1994
APS Manuscript Number C0556-3.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.