Comparative Studies on the Mineralo-Corticoid Action of Aldosterone and Carbenoxolone Sodium in the Adrenalectomized Rat

Abstract

Carbenoxolone sodium at 10 mg/kg when given subcutaneously to adrenalectomized rats, does not show a retention of urinary sodium ion comparable to that observed with 0.2 μg/rat (1.0 μg/kg) of aldosterone, nor does carbenoxolone sodium at 10 mg/kg show any significant increase of urinary potassium excretion, whereas, under the same conditions, a significant increase in potassium excretion was observed with aldosterone at 0.2 μg/rat. At a higher dose of carbenoxolone sodium 50 mg/kg, which is comparable to 10 times the clinical dose in man, sodium retention and increased potassium excretion was observed which was significantly different from control animals but less than that observed for 2.0 μg of aldosterone. In similar experiments, no potentiation of aldosterone effects was observed when carbenoxolone sodium at 10 mg/kg was given concomitantly with aldosterone at 0.2 μg/rat (1.0 μg/kg). The present experiments confirm the anti-natriuretic action of carbenoxolone sodium but failed to demonstrate any enhancement of the mineralocorticoid action of aldosterone by carbenoxolone sodium.

Central hypertensinogenic effects of glycyrrhizic acid and carbenoxolone

“…While most reported studies indicate that carbenoxolone does not affect the mineralocorticoid activity of aldosterone (25), others suggest that it enhances the sodium retention produced by aldosterone and ll-deoxycorticosterone (23). Glycyrrhetinic acid has been found to inhibit the hepatic 5P-reductase and 3P-HSD but not the 5a-reductase or 3cu-HSD.…”