Fatty acid binding protein of cardiac muscle in spontaneously hypertensive rats: effect of hypertrophy and its regression.

To investigate the relationship between cardiac hypertrophy associated with hypertension, and the alterations in myocardial lipid metabolism, nicardipine (160 mg/kg/day), hydralazine (40 mg/kg/day), and enalapril (30 mg/kg/day) were administered to spontaneously hypertensive rats from 20 to 24 weeks of age. Drug administration significantly suppressed the increases in blood pressure and the ratio of left ventricular weight to body weight. A marked variation in the fatty acid binding capacities of the delipidated, dealbuminated heart cytosol obtained from these animals was observed in the 24-week-old rats (5.40 +/- 0.31 pmol/micrograms protein in non-treated rats; 4.73 +/- 0.34 pmol/mg protein in nicardipine-treated rats; 5.01 +/- 0.34 pmol/mg protein in hydralazine-treated rats; 4.61 +/- 0.26 pmol/mg protein in enalapril-treated rats) as compared to the 20-week-old non-treated rats (3.38 +/- 0.29 pmol/mg protein). The decrease in this capacity in the drug-treated groups closely correlated with the reduction of cardiac mass, suggesting that the factors governing regression may be closely related to those governing fatty acid binding capacity. It appears that fatty acid binding protein may play an important role in the hypertension-associated hypertrophic myocardium.