Abstract
In general, it is recognized that prolonged exposure to catecholamine leads to a reduction in the β-adrenoceptor density (downregulation). However, it has been previously reported that the myocardial β-adrenoceptor densities and norepinephrine levels significantly increase in the hearts of BIO 14.6 cardiomyopathic hamsters in the early stage. The mechanism of the increased β-adrenoceptor density is not clearly elucidated, and it can not be excluded that this phenomenon may be a secondary effect. The purpose of this study was to assess the effect of verapamil on the density of β-adrenoceptors in the heart of BIO 14.6 cardiomyopathic hamsters. The total number of β-adrenoceptors in untreated BIO 14.6 hamsters was significantly higher at 90 days of age (30.4±2.2 v.s. 25.9±1.4 fmol/mg protein, p<0.05). BIO 14.6 hamsters received daily intraperitoneal injections of 5 mg/kg verapamil for 70 days, from an age of 20 days. Verapamil protected against progressive myocardial damage (total damage; 8.2±0.7 v.s. 0.4±0.2%/area, p<0.05) and the myocardial β-adrenoceptor density returned to that of the normal control group (26.9±3.0 fmol/mg protein). Conversely, verapamil did not have an effect on the number of myocardial β-adrenoceptors in normal golden hamsters. This study showed that verapamil protected against progressive myocardial damage and myocardial β-adrenoceptor density returned to those of normal hamsters. These results suggest that an increased number of β-adrenoceptors in the early stage of BIO 14.6 cardiomyopathic hamsters may be involved in the secondary pathogenesis of cardiomyopathy.
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Kobayashi, A., Nishiyama, T., Ikegaya, T. et al. Verapamil induced reduction of the myocardial β-adrenoceptor density in BIO 14.6 cardiomyopathic Syrian hamsters. Mol Cell Biochem 121, 59–65 (1993). https://doi.org/10.1007/BF00928700
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DOI: https://doi.org/10.1007/BF00928700