Effect of carbenoxolone sodium on steroid-induced sodium transport in the toad bladder: further studies.

The licorice derivative, carbenoxolone sodium, is a potent inhibitor of the enzyme 11 beta-hydroxysteroid dehydrogenase. When this enzyme is suppressed or is absent, endogenous glucocorticoids induce mineralocorticoid-like sodium retention by the kidney. Carbenoxolone sodium administered in vivo to an adrenalectomized rat has also recently been shown to enhance the mineralocorticoid response to submaximal concentrations of aldosterone, deoxycorticosterone (DOC) and 11-dehydrocorticosterone (compound A). In the present studies conducted on the urinary bladder isolated from the Dominican toad, Bufo marinus, a concentration of carbenoxolone sodium shown previously to increase glucocorticoid-induced sodium transport (2.5 x 10(-5) M) did not appear to alter the response to submaximal concentrations of aldosterone 10(-8) M, DOC 10(-7) M, or compound A 10(-5) M. These findings are consistent with the view that in the whole animal carbenoxolone sodium may modify additional steroid metabolic pathways and/or physiological processes in several organs to produce the enhanced renal response to mineralocorticoids and compound A.