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Division of Renal Diseases and Hypertension, Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455; and National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892
Submitted 27 March 2003 ; accepted in final form 10 January 2004
Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-
1 (TGF-) and scarring in many such models, we hypothesized that aldosterone could evoke TGF- in the kidney. Aldosterone infusion for 3 days in otherwise normal rats caused a more than twofold increase in TGF- excretion without changes in systolic pressure or evidence of kidney damage. Concurrent treatment with amiloride did not alter this effect, indicating that aldosterone's stimulation of TGF- was independent of its regulation of sodium or potassium transport. However, concurrent treatment with spironolactone did block the increase in TGF-, indicating that the effect depends on the mineralocorticoid receptor. Renal mRNA for serum glucocorticoid kinase rose, but no change in TGF- message occurred, suggesting posttranscriptional enhancement of renal TGF-. In summary, aldosterone provokes renal TGF-, and this action may contribute to aldosterone's fibrotic propensity.
aldosterone; transforming growth factor-; kidney
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