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Effect of Aldosterone and Glycyrrhetinic Acid on the Protein Expression of PAI-1 and p22^phox in Human Mononuclear Leukocytes

Department of Clinical and Experimental Medicine, Clinica Medica 4 (L.A.C., F.Z., E.P., P.D.M.) and Department of Medical and Surgical Sciences, Endocrinology (P.S., G.M., C.F., D.A.), University of Padua, Padua 35100, Italy; Departments of Nutrition, Epidemiology and Preventive Medicine (P.A.D.), University of California-Davis, Davis, California 95616

Address all correspondence and requests for reprints to: Decio Armanini, M.D., Department of Medical and Surgical Sciences, Via Ospedale 105, Padua 35100, Italy. E-mail: decius{at}libero.it.

Abstract

Aldosterone excess can produce heart and kidney fibrosis, which seem to be related to a direct effect of aldosterone at the level of specific receptors. We report a direct, mineralocorticoid-mediated effect on the protein expression of two markers of oxidative stress after incubation of mononuclear leukocytes with 1 x 10^–8 M aldosterone (p22^phox/ß-actin = 1.38 ± 0.05 and PAI-1/ß-actin = 1.80 ± 0.05). The same effect was also found with 3 x 10^–5 M glycyrrhetinic acid, the principal constituent of licorice root (p22^phox/ß-actin = 1.37 ± 0.97 and PAI-1/ß-actin = 1.80 ± 0.04). The effect of both aldosterone and glycyrrhetinic acid is blocked by incubation with added 1 x 10^–6 M of receptor-antagonist canrenone. Canrenone alone did not show any effect. PAI-1 related protein was also found using 4 x 10^–9 M aldosterone. Incubations with 1 x 10^–9 M for 3 hours as well as 1 x 10^–8 M aldosterone for 5, 10, and 20 minutes were ineffective for both proteins. These data support the previous finding of an involvement of mononuclear leukocytes in the pathogenesis of the oxidative stress induced by hyperaldosteronism. In addition, the results confirm our previous data on a direct effect of glycyrrhetinic acid at the level of mineralocorticoid receptors.

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