PROPRANOLOL AND BEPRIDIL ATTENUATING LEVOTHYROXINE-INDUCED RAT CARDIAC-HYPERTROPHY AND MITOCHONDRIAL CA2-ATPASE ACTIVITY ELEVATION( MG2+)

AIM: To study the effects of propranolol and bepridil on levothyroxine -induced rat cardiac hypertrophy and mitochondrial Ca2+ Mg2+-ATPase ac tivity, elevation. METHODS: Rat heart hypertrophy was induced by ip le vothyroxine 1 mg . kg(-1). d(-1) x 10 d. Their rats were treated by ig propranolol (Pro) or bepridil (Bep) 10 mg . kg(-1) daily. Ca2+ Mg2+-A TPase activity and enzyme kinetic parameters were assayed. RESULTS: Th e activity and V-max of mitochondrial Ca2+ Mg2+-ATPase isolated from h ypertrophic left ventricle were 25 +/- 4 and 35.1 +/- 0.8 mu mol P-i . h(-1)/mg protein, respectively, those of normal were 6.7 +/- 1.8 and 10 +/- 4 mu mol P-i . h(-1)/mg protein, respectively. Apparent K-m of the hypertrophic group Ca2+ Mg2+-ATPase was 0.4 +/- 0.12 mmol . L(-1) ATP, and that of normal was 0.59 +/- 0.22 mmol . L(-1) ATP. The total protein quantity of hypertrophic left ventricle was 80 +/- 30 mg, and that of normal was 47 +/- 9 mg. After treated with Pro or Bep (both 10 mg . kg(-1) ig), the cardiac hypertrophy was attenuated, the enzyme a ctivity and V-max as well as total protein quantity of hypertrophic le ft ventricle were reduced to normal level, but apparent K-m was not af fected. CONCLUSION: Both Pro and Bep prevented the myocardium and its mitochondria from ischemia and overload calcium injury.