Abstract
Effects of captopril and hydralazine on the cardiac β-adrenoceptor pathway in chronic heart failure were investigated. After myocardial infarction (MI) had been experimentally induced in rats, captopril (Cap) or hydralazine (Hyd) was administrated orally for four weeks. Then β-adrenoceptor density (Bmax) and cAMP yield, by either isoproterenol (ISO) -or forskolin-stimulation, were determined. Bmax was significantly increased in MI (N) rats (rats with MI without treatment) as compared with sham-operated rats (63.0 ± 4.6 vs. 38.8±4.4fmol/mg prot. : p<0.05). Cap-treatment of MI had no effect on receptor density (61.8±5.1fmol/mg prot.). On the other hand, Hyd-treatment of MI significantly increased Bmax (92.8 ± 4.6 : p< 0.01). The cAMP yield of MI (N) significantly declined as compared with that of sham operated rats. Both treatments, Cap or Hyd, increased cAMP yield following ISO-stimulation, but cAMP remained unchanged following forskolin-stimulation. Thus, in chronic heart failure due to myocardial infarction, the reactivity of myocytes to catecholamine deteriorate in spite of the increase in β-adrenergic receptor density. This is due to neither increasing receptor density nor improving the activity of the catalytic unit of adenylate cyclase. Captopril seems to improve the activity of G-protein. This regulatory effect of captopril in heart failure is different from that of hydralazine.
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