TITLE

Lithium-induced ADH resistance in toad urinary bladders

AUTHOR(S)
Singer, Irwin; Franko, Elizabeth A.
PUB. DATE
January 1973
SOURCE
Kidney International;Jan1973, Vol. 3 Issue 1, p151
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
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.
ACCESSION #
18287614

 

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