The myocardium contains myocyte and non-myocyte cells. A disproportionate growth of the nonmyocyte cell population can alter myocardial structure and lead to pathologic hypertrophy. Myocardial fibrosis, the result of cardiac fibroblast growth or abnormal accumulation of fibrillar collagen within the interstitial space, can adversely influence myocardial stiffness and ultimately ventricular function. We have examined the relative importance of ventricular systolic and arterial pressures and the effector hormones of the renin-angiotensin--aldosterone system in mediating this reactive fibrous tissue response in the hypertensive left and normotensive right ventricles in various experimental models of arterial hypertension. To date, our findings implicate arterial hypertension, together with an elevation in plasma aldosterone, as being contributory to the fibrosis in renovascular hypertension that creates tissue heterogeneity in either ventricle and impaired diastolic function. The endocrine properties of aldosterone in this nonclassical mineralocorticoid target tissue, the myocardium, requires further investigation.