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  • Title: Cytoplasmic phosphates in Na(+)-K+ balance in KCN-poisoned rat heart: a 87Rb-, 23Na-, and 31P-NMR study.
    Author: Kupriyanov VV, Yang L, Deslauriers R.
    Journal: Am J Physiol; 1996 Apr; 270(4 Pt 2):H1303-11. PubMed ID: 8967370.
    Abstract:
    The effect on intracellular Na+ ([Na+]i) and Rb+ fluxes if reduced [ATP]/ [ADP] and increased Pi has been investigated by 1 mM potassium cyanide (KCN) or KCl (control) infusion (24 min) in Langendorff perfused rat hearts. 87Rb, 23Na, or 31P nuclear magnetic resonance (NMR) 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 microM) 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 glibenclamide (Glib, 10 microM. 0.042 +/- 0.009, P = 0.0001 vs. KCN) and alpha-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 Glib (47 +/- 17%, P = 0.03). We suggest that inhibition of Na(+)-K(+)-adenosinetriphosphatase (ATPase) by Pi is responsible for intracellular Na+ 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.
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