AJP - Heart and Circulatory Physiology, Vol 244, Issue 2 247-H252, Copyright © 1983 by American Physiological Society
Sodium dependence of carnitine transport in isolated perfused adult rat hearts
T. C. Vary and J. R. Neely
In heart muscle, the intracellular carnitine concentration is approximately
40 times higher than the plasma carnitine concentration, suggesting the
existence of an active transport process. At physiological serum carnitine
concentrations (44 microM), 80% of total myocardial carnitine uptake occurs
via a carrier-mediated transport system. The mechanism of this
carrier-mediated transport was studied in isolated perfused rat hearts.
Carnitine transport showed an absolute dependence on the extracellular
sodium concentration. The rate of carnitine transport was linearly related
to the perfusate sodium concentration at every perfusate carnitine
concentration examined (15-100 microM). Total removal of extracellular
sodium completely abolished the carrier-mediated transport. Decreasing the
perfusate potassium concentration from a control of 5.9 to 0.6 mM
stimulated transport by 35%, whereas increasing the extracellular potassium
concentration from 5.9 to 25 mM reduced transport by 60%. The
carrier-mediated transport was inversely proportional to the extracellular
potassium concentration. Acetylcholine (10(-3) M), isoproterenol (10(-7)
M), or ouabain (10(-3) did not alter the rate of carnitine transport.
Addition of tetrodotoxin (10(-5) stimulated carnitine transport by about
40%, while gramicidin S (5 X 10(-6) M) decreased uptake by about 18%
relative to control. The data provide evidence that carnitine transport by
cardiac cells occurs by a Na+-dependent cotransport mechanism that is
dependent on the Na+ electrochemical gradient.
