This study was designed to determine whether thyroid hormone (T4) produces cardiac hypertrophy and alters ventricular function by direct effects on the heart or by alterations in adrenergic stimulation or changes in the peripheral circulation. Rats were treated with captopril (4 mg/ml of drinking water), propranolol (0.5 mg/ml of drinking water), hydralazine (80 mg/l of drinking water) or the combination of captopril and propranolol with and without T4 (15 μg/100 g b.w. i.p.). After 10 days, T4 increased (P<.01) heart rate, left ventricular (LV) dP/dt and LV weight/body weight, but did not alter LV systolic pressure (SP) or end-diastolic pressure (EDP). Compared to treatment with T4 alone, captopril plus T4 decreased LV SP (P<.05) and LV EDP (P<.01); however, heart rate, LV dP/dt and LV weight/body weight were unchanged. Treatment with T4 plus propranolol decreased heart rate and LV EDP (P<.05) compared to T4 alone; however, LV SP, LV dP/dt and LV weight/body weight were unchanged (P>.05). Hydralazine did not alter (P>.05) heart rate, LV SP, LV EDP or prevent the development of increased LV weight/body weight when given with T4; however, LV dP/dt was slightly decreased (P<.05). Treatment with the combination of captopril and propranolol did not alter (P>.05) heart rate, LV SP, LV EDP or LV dP/dt and also failed to prevent the development of increased LV weight/body weight and LV dP/dt when given with T4. Thus, LV hypertrophy and augmentation of LV function were produced by T4 treatment despite beta adrenoceptor blockade with propranolol, alteration of cardiac load with captopril or hydralazine and the combination of beta adrenoceptor blockade and captopril.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Molecular Medicine