The role of cytoplasmic phosphates in na+/k+ imbalance caused by
kcn in perfused rat heart: a 87rb, 23na and 31p nmr study.
Kupriyanov, V. V., L. Yang, and R. Deslauriers.
Institute for Biodiagnostics, National Research Council Canada,
Winnipeg, MB, Canada
APStracts 2:0454H, 1995.
The effect on [Na+]i and Rb+ fluxes of reduced [ATP]/[ADP] and
increased Pi has been investigated by 1 mM KCN or KCl (control)
infusion (24 min) in Langendorff perfused rat hearts. 87Rb, 23Na or
31P MR spectra were acquired to measure intracellular Rb+ (a congener
for K+, 20% substitution), Na+ and phosphates. KCN infusion (14-24
min) caused decreases in phosphocreatine (34 12% of initial), ATP (64
17) and Rb content (71 7) and increases in Pi (273 65) and [Na+]i
(210 52). Dimethylamiloride (10 M) did not change the rate of Na+
accumulation. The rate constant of unidirectional Rb+ efflux (min-1)
increased during KCN treatment by 70% (0.061 0.006, vs. 0.036 0.004,
p=0.0001). KCN-stimulated Rb+ efflux was inhibited by glybenclamide
(Glyb, 10 M, 0.042 0.009, p=0.0001 vs. KCN) and a-cyano-4
-hydroxycinnamate (0.5 mM, 0.047 0.008, p<0.002 vs. KCN). KCN
moderately decreased the Rb+ influx rate (to 82 17%, p=0.01) which
was depressed more significantly in the presence of Glyb (47 17%,
p=0.03). We suggest that inhibition of Na+/K+ ATPase by Pi is
responsible for Na+i accumulation, whereas K+ loss is associated with
both activation of ATP-sensitive K+ channels and the K+/Lactate-
cotransporter and inhibition of Na+/K+ ATPase.
Received 10 July 1995; accepted in final form 8 September 1995.
APS Manuscript Number H637-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95