Protein remodelling of the heart in NO-deficient hypertension: the effect of captopril
Abstract
Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of NO-deficient hypertension. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril can prevent hypertension, left ventricular (LV) hypertrophy, changes in nucleic acid concentration, protein synthesis and protein profile of the left ventricle. Four groups of rats were investigated: control, L-NAME 40 mg/kg/day, captopril 100 mg/kg/day, L-NAME 40 mg/kg/day along with captopril 100 mg/kg/day. NO-synthase activity in the left ventricle was found to be decreased by 69% in the L-NAME group. Captopril did not influence this inhibition of NO-synthase activity. However, it completely prevented hypertension and left ventricular hypertrophy development. The increase in left ventricular RNA and DNA concentration and -14C-leucine incorporation observed in the L-NAME group was completely prevented by simultaneous captopril treatment. The protein profile of the left ventricle in the L-NAME group was characterized by higher concentration of metabolic proteins (MP), soluble collagenous proteins (SCP) and of hydroxyproline in insoluble collagenous proteins (ICP). The concentration ...Continue Reading
Citations
Comparison of the effects of indapamide and captopril on the development of spontaneous hypertension
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