AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 593-H598, Copyright © 1985 by American Physiological Society
Erythrocyte adenosine transport: effects of Ca2+ channel antagonists and ions
D. A. Ford, J. A. Sharp and M. J. Rovetto
On the basis of observations of adenosine-Ca2+ competition, we assessed the
effects on erythrocyte adenosine transport of Ca2+ channel antagonists,
mono- and divalent cations, and Cl- and Cl- transport inhibitors. The Ca2+
channel antagonists, diltiazem and verapamil, competitively inhibited
adenosine influx (Ki = 158 +/- 17.4 and 13.5 +/- 1.3 microM at 10 microM
adenosine, respectively), despite no apparent effect on transport by Ca2+,
Mg2+, Na+, or K+. Verapamil also inhibited uridine efflux (Ki = 1.7 +/- 0.3
microM at 84-100 microM intracellular uridine). The absence of Cl-
decreased adenosine influx rates from 0.615 +/- 0.013 to 0.386 +/- 0.008
nmol X s-1 X ml intracellular H2O-1. The Cl- transport inhibitors,
diisothiocyanostilbene disulfonate (10 microM), furosemide (1 mM), and NO-3
(145 mM), decreased adenosine influx rates to 0.301 +/- 0.008, 0.325 +/-
0.013, and 0.430 +/- 0.009 nmol X s-1 X ml intracellular H2O-1,
respectively. These studies indicate that the Ca2+ channel antagonists
inhibit adenosine release and uptake and therefore may modulate
adenosine-mediated events. Additionally, they suggest that adenosine and
anion transport systems are linked or share common features.
