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1 Previous in vivo studies in men and experimental animal models have shown that hyperaldosteronemia is correlated with cardiac ®brosis due to increased total collagen synthesis. As yet, it is unclear whether aldosterone has direct pro-®brogenic e ect on cardiac ®broblasts, the ®brogenic e ector cell in the myocardium, and if so which procollagens speci®cally are synthesized at higher rates. 2 The present study aims at establishing whether de novo collagen synthesis by cardiac ®broblasts is enhanced following exposure for 2624 h to pharmacological (10 77 ± 10 78 M), near-physiological (10 79 M) or physiological (10 710 ± 10 711 M) aldosterone concentrations. During the last 24 h, cells were metabolically labelled with [ 35 S]-methionine/[ 35 S]-cysteine. Labelled procollagens were immunoprecipitated quantitatively using antibodies against speci®c procollagens. Contrary to expectations, 10 77 M aldosterone inhibited signi®cantly de novo synthesis of procollagens type I and IV (735% and 742%, respectively). For procollagen type III, only a tendency towards inhibition was observed. At lower concentrations of aldosterone (10 78 ± 10 710 M), synthesis of procollagens type I, III or IV was una ected. 3 Cellular DNA synthesis under in¯uence of aldosterone was evaluated by measuring BrdU incorporation. Cells were treated with aldosterone, while BrdU was added during the last 16 h of treatment. Aldosterone had no demonstrable e ect on cellular proliferation. 4 Reverse transcription-polymerase chain reaction (RT ± PCR) clearly demonstrated the presence of mineralocorticoid receptor mRNA in cardiac ®broblasts. 5 In spite of the expression of the mineralocorticoid receptor by cultured cardiac ®broblasts, the pro-®brogenic e ect of aldosterone as observed in vivo, is not likely to be due to a direct e ect of this hormone in cardiac ®broblasts.