Abstract

The distribution and transmembrane fluxes of 28Mg were examined in the isolated media-intimal layer of rabbit aorta. Accumulation of 28Mg was slow and not complete after a 3-hr incubation. The major portion of the cellular Mg++ is not exchangeable. The 28Mg efflux rate was increased by 1.5 mM nonradioactive Mg++ after a time lag of 5 to 10 min; this increase was blocked reversibly by decreasing bathing solution temperature to 4 degrees C. A rapid and sustained increase in 28Mg efflux rate was elicited with added EDTA. Accumulation of 28Mg by rabbit aorta was increased more than 5-fold by substituting sucrose for NaCl in the bathing solution. Q10 values obtained for Mg++ accumulation in rabbit aorta incubated at different temperatures either in normal solution or low-Na+ solution ranged from 1.3 to 2.0. Uptake of 28Mg was inhibited substantially by 60 mM added K+, 1.5 or 15.0 mM La , 7 mM neomycin or 1 microgram/ml of antimycin A. These ions and drugs did not significantly increase 28Mg efflux when added during the slow component phase of the washout. Thus, the major portion of slowly accumulated Mg++ appears to be stored and exchanged intracellularly. The transmembrane movements of Mg++ depend upon simple diffusion, Mg++-Mg++ exchange and a transport process that is increased when Na+ is decreased. The EDTA-induced increase in 28Mg efflux rate may result from nonspecific membrane permeability increases, whereas ions and drugs decrease cellular Mg++ content by reducing uptake rather than increasing loss.