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The β2-agonist clenbuterol [4-amino-α(t-butyl-amino)methyl-3,5-dichlorobenzyl alcohol] is used as a non-steroidal anabolic drug for sports doping. The effects of clenbuterol on the transcriptional process and mRNA stability of β-adrenoceptor (β-AR) in skeletal and cardiac muscles are still unknown. Therefore, we investigated the effects of clenbuterol on β1- and β2-AR mRNA expressions of fast-twitch fiber–rich extensor digitorum longus (EDL), slow-twitch fiber–rich soleus (SOL), and left ventricle (LV) muscles by real-time RT-PCR. Adult male Sprague Dawley rats were divided into the clenbuterol-administered group and control group. The administration (dose = 1.0 mg/kg body weight/day, s.c.) of clenbuterol was maintained for 10 days. The administration of clenbuterol significantly increased the weight, RNA concentration, and total RNA content of EDL muscle. No effects of clenbuterol on those of SOL and LV muscles, however, were observed. The administration of clenbuterol significantly decreased β1-AR mRNA expression of LV muscle. Furthermore, the administration of clenbuterol significantly decreased β2-AR mRNA expression of EDL and LV muscles. No effect of clenbuterol on β2-AR mRNA expression of SOL muscle, however, was observed. These results suggest that the effects of clenbuterol on β1- and β2-AR mRNA expressions and muscle hypertrophy depend on muscle fiber types. Keywords:: clenbuterol, β-adrenoceptor mRNA, down-regulation, muscle hypertrophy, skeletal and left ventricle muscles

Clenbuterol [CLE: 4-amino-α(t-butyl-amino)methyl-3,5-dichlorobenzyl alcohol] is well known as a potent β2-adrenergic agonist and non-steroidal anabolic drug, and thus it is generally used for sports doping and asthma therapy. Although the functions of immune cells such as white blood cells (WBCs) have shown to be modulated through β2-adrenoceptors, the effects of CLE on immune-responsive systems have not been elucidated systematically. Therefore, the effects of CLE on the number of WBCs were studied in rats. Male adult rats were divided into CLE-administered group and the control group to compare the number of total WBCs, neutrophils, monocytes, lymphocytes, eosinophils, and basophils. The administration (dose = 1.0 mg ⋅ kg−1 body weight ⋅ day−1, s.c.) of CLE was maintained for 30 days. CLE did not change the number of total WBCs during the experimental period. However, CLE increased significantly the number of neutrophils and monocytes, while CLE decreased drastically the number of lymphocytes and eosinophils. There was no significant change in the number of basophils between both groups. These results suggest that the administration of CLE induces drastic redistribution of WBCs in circulation without changing the number of total WBCs, and these responses of WBCs during the administration of CLE are sustained for at least 30 days. Keywords:: β2-agonist, clenbuterol, immune-responsive system, white blood cell, lymphocyte