Lithium-induced ADH resistance in toad urinary bladders

Singer, Irwin; Franko, Elizabeth A.
January 1973
Kidney International;Jan1973, Vol. 3 Issue 1, p151
Academic Journal
The toad urinary bladder was used to investigate the site of action, the underlying mechanism, and the means for production or prevention of lithium-induced nephrogenic diabetes insipidus. Short-circuit current (I) was used to measure net sodium transport in paired quarter-bladders. Osmotic water flow (W) was measured both volumetrically and gravimetrically. Mucosal [Li+] at 11 mEq/liter produced inhibition of baseline I and both ADH-induced cAMP-mediated I and W. However, lithium did not inhibit propionate-induced I, or either dibutyryl cAMP-induced I or W, confirming that lithium acts primarily by inhibition of ADH-induced, cAMP-mediated responses. Serosal lithium had no effect at these concentrations. Either amiloride (10-6M) or triamterene (10-5M) prevented all lithium inhibition, proving that lithium acts from the mucosal surface. Increased urinary [K+] or [H+] prevented lithium inhibition of ADH-induced responses, suggesting that urinary composition may be important in both production and prevention of lithium-induced nephrogenic diabetes insipidus.


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