Several studies have reported that chronic β-adrenergic stimulation is associated with functional cardiac alterations as well as ventricular hypertrophy. It is well known that aldosterone is a profibrotic factor which participates in the development of ventricular hypertrophy and heart failure. However, the participation of aldosterone in cardiac alterations produced by chronic stimulation of β-adrenergic receptors is not established. Therefore, the aim of this study was to evaluate the cardiac effects of an antagonist of mineralocorticoid receptors in rats with chronic stimulation of β-adrenergic receptors. To this end, male Wistar rats (250g), N=6 in each group, were treated with either isoproterenol (ISO; 3mg/kg/day s.c.) or vehicle for 15 days. Half of the animals from each group were treated with spironolactone (SPIRO; 200mg/Kg/day s.c). At the end of the treatment, heart rate (HR) was measured. In addition, systolic arterial pressure (SAP), diastolic (DAP) and mean (MAP), left ventricle final diastolic pressure (pDf), + dP/dt and – dP/dt were measured through a catheter inserted into the right carotid artery. Animals were anesthesiced with ketamine (0.07ml/100mg body weight) and Xilacyne (0.03ml/100mg corporal weight) by intraperitoneal injection. Also, cardiomyocytes diameter and collagen content present in the miocardium was evaluated with optical microscopy techniques. As index of cardiac hypertrophy, the ratio heart/body weight was calculated. Neither ISO nor SPIRO were able to modify SAP, DAP, MAP, HR, + dP/dt y – dp/dt. However, pDf was higher (p<0.001) in rats treated with ISO as compared with controls. Treatment with SPIRO normalized these values (p<0.001). Relative heart weight was greater in the rats treated with ISO (p<0.001) than in controls. Treatment with SPIRO reduced heart weight (p<0.01) without becoming normalized. No differences in cardiomyocyte diameter were observed in any group. Collagen content in the myocardium of rats treated with ISO was greater (p<0.001) than in control rats. Treatment with SPIRO reduced collagen content (p<0.05) without reaching levels observed in controls. In conclusion, these data suggest that chronic stimulation of β-adrenergic receptors in rats induces diastolic dysfunction and cardiac hypertrophy associated with an increase in extracellular matrix. Aldosterone participates in these alterations.