The 11 beta-OHSD inhibitor, carbenoxolone, enhances Na retention by aldosterone and 11-deoxycorticosterone.
Carbenoxolone sodium, CS, a liquorice derivative associated with hypertension and sodium retention, has been demonstrated to inhibit 11 beta-hydroxysteroid dehydrogenase, an enzyme that metabolizes cortisol and corticosterone to their respective inactive 11-dehydro products (cortisone and 11-dehydrocorticosterone). It has been proposed that the increased bioavailability of unmetabolized corticosterone and cortisol following 11 beta-OHSD inhibition allows these steroids to act on renal mineralocorticoid receptors to elicit the mineralocorticoid action. Here we describe how CS amplifies the antinatriuretic activity of aldosterone and deoxycorticosterone; the latter steroid is of particular importance in that it does not possess a hydroxyl group at the C-11 position in the steroid ring, indicating that another mechanism(s) in addition to 11 beta-OHSD inhibition is responsible for the amplification of the action of deoxycorticosterone.[1]References
- The 11 beta-OHSD inhibitor, carbenoxolone, enhances Na retention by aldosterone and 11-deoxycorticosterone. Morris, D.J., Souness, G.W. Am. J. Physiol. (1990) [Pubmed]
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