Abstract
The potential dependence of ouabain inhibition of sodium transport in toad bladder was examined by maintaining the transepithelial potential difference at different values with a voltage clamp device during ouabain administration. Inhibition of sodium transport was assessed by intermittent observation of spontaneous potential difference (PD) and short-circuit current. In continuously hyperpolarized bladders, ouabain was relatively ineffective as an inhibitor of spontaneous PD and short-circuit current: a concentration of 10-3 M produced only 20% inhibition. In continuously short-circuited bladders, by contrast, 10-5 M ouabain produced 20 to 30% inhibition, whereas 10-3 M ouabain nearly abolished PD and short-circuit current. Results in open-circuited bladders were only slightly different from those in short-circuited preparations, but bladders in which PD was clamped at its initial value and thus was prevented from falling, were intermediate. To some extent, these effects were reversible; hyperpolarization of bladders inhibited by ouabain during short-circuiting led to partial recovery. In a second series of experiments, bidirectional sodium fluxes were measured before and after adding graded doses of ouabain to short-circuited, open-circuited or hyperpolarized bladders. The dosage of drug required to produce reduction of net mucosal-to-serosal transport in these three conditions were 10-6, 10-4 and ≤ 10-3 M, respectively. The results indicate that the susceptibility of the sodium pump in toad bladder to inhibition by ouabain varies at least 100-fold with the magnitude of transepithelial potential. Possible mechanisms are discussed.
Footnotes
- Received September 25, 1972.
- Accepted January 3, 1973.
- © 1973 by The Williams & Wilkins Co.
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