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The Journal of Membrane Biology

, Volume 28, Issue 1, pp 121–142 | Cite as

Effects of 2-deoxy-d-glucose, amiloride, vasopressin, and ouabain on active conductance andENa in the toad bladder

  • C. D. Hong
  • A. Essig
Article

Summary

The effects of various agents on active sodium transport were studied in the toad bladder in terms of the equivalent circuit comprising an active conductanceKa, an electromotive forceENa, and a parallel passive conductanceKp. For agents which affectKa, but notENa orKp, the inverse slope of the plot of total conductance κ against short-circuit currentI0 evaluatesENa, and the intercept representsKp. Studies employing 5×10−7m amiloride to depressKa indicate a changingENa, invalidating the use of the slope technique with this agent. An alternative suitable technique employs 10−5m amiloride, which reducesI0 reversibly to near zero without effect onKp. Despite curvilinearity of the κ-I0 plot under these conditions,Kp may therefore be estimated fairly precisely from the residual conductance. It then becomes possible to follow the dynamic behavior ofKa andENa (in the absence of 10−5m amiloride) by frequent measurements of κ andI0, utilizing the relationshipsKa=K-Kp, andKNa=IO/(K-Kp). 2-deoxy-d-glucose (7.5×10−3m) depressedKa without affectingENa. Amiloride (5×10−7m) depressedKa and enhancedENa. Vasopressin (100 mU/ml) enhancedKa markedly and depressedENa slightly. Ouabain (10−4m) depressed bothKa andENa. All of the above effects were noted promptly;Kp was unaffected. The “electromotive force of Na transport”ENa appears not to be a pure energetic parameter, but to reflect kinetic factors as well, in accordance with thermodynamic considerations.

Keywords

Active Sodium Vasopressin Equivalent Circuit Ouabain Frequent Measurement 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag New York Inc. 1976

Authors and Affiliations

  • C. D. Hong
    • 1
  • A. Essig
    • 1
  1. 1.Department of PhysiologyBoston University School of MedicineBoston

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