Using a special Millar ultraminiature catheter pressure transducer, right ventricular functional parameters were measured in anesthetized, closed-chest rats under control conditions, during acute pulmonary hypertension and after induction of right ventricular hypertrophy. Acute i.v. infusion of noradrenaline and a brief period of hypoxia in female Sprague-Dawley rats elicited a marked increase in right ventricular systolic pressure (RVSP) and in the maximal rate of rise in right ventricular pressure (RV dp/dtmax). After 3 and 16 days of daily administrations of triiodothyronine in female Sprague-Dawley rats, all right ventricular hemodynamic parameters were enhanced along with the increase in left ventricular function. The right and left ventricles were hypertrophied, and cardiac output was increased. After 40 and 45 days subsequent to bilateral thorax irradiation of male Brown-Norway rats, RVSP and RV dp/dtmax were increased, the right ventricle was hypertrophied, while the left ventricle did not exhibit appreciable hemodynamic or morphologic alterations. Cardiac output was depressed. Thus, these two experimental models differ considerably as to the mechanism and time course of the development of right ventricular hypertrophy as well as to the participation of the left ventricle and the involvement of volume overload.