Tolerance to or facilitation of pharmacological effects induced by chronic treatment with the beta-adrenergic stimulant clenbuterol

Frances, Henriette; Diquet, Bertrand; Goldschmidt, Pablo; Simon, Pierre

doi:10.1007/bf01260416

Cited by 10 publications

(2 citation statements)

References 30 publications

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“…anabolic adrenergic agonist; cardiomyocytes; sympathomimetic; necrosis; immunohistochemistry; ␤-adrenergic antagonists THE ANABOLIC AND LIPOLYTIC EFFECTS of the ␤ 2 -adrenergic receptor (AR) agonist clenbuterol have been widely investigated, principally at doses ranging from 1 to 5 mg/kg in a variety of sedentary laboratory and livestock animals (6,12,25,29). In response to such doses, the size of the heart, skeletal muscle, bone, lung, and kidney all increase, whereas the liver (35) and adipose tissue decrease in mass (6,30).…”

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confidence: 99%

Myotoxic effects of clenbuterol in the rat heart and soleus muscle

Burniston

Clark

et al. 2002

Journal of Applied Physiology

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Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.

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Myotoxic effects of clenbuterol in the rat heart and soleus muscle

Burniston

Clark

et al. 2002

Journal of Applied Physiology

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“…Chronic administration of the g-agonist, clenbuterol, produced tolerance to decreased locomotor activity and reduced investigation of food whereas antagonism of reserpine induced hypothermia and potentiation of yohimbine toxicity were enhanced (14).…”

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confidence: 99%

Effects of Ibuterol, a β-2 Adrenergic Prodrug, on Intraocular Pressure

Phipps

Potter²,

Rowland³

1986

Journal of Ocular Pharmacology and Therapeutics

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Ibuterol, a prodrug of terbutaline, was approximately 100 times more potent than terbutaline in producing ocular hypotension in the treated eye of normal and sympathectomized (SX) rabbits. In normal rabbits, ibuterol produced no change in IOP of the contralateral eye whereas in unilaterally SX rabbits a rise in IOP occurred in the SX (contralateral) eye when the normal eye was treated with ibuterol.Ibuterol also suppressed ocular hypertension induced by water loading and delayed the IOP recovery rate although its onset of action was delayed. Aqueous flow was increased significantly at 1 hr after ibuterol in fluorophotometric studies in normal rabbits. Pretreatment with forskolin antagonized rather than enhanced ibuterol-induced ocular hypotension. Pretreatment with diclofenac failed to suppress the development of tachyphylaxis to the ocular hypotensive effect of ibuterol. Although ibuterol is an effective ocular hypotensive agent in rabbits, the effects of this agent on aqueous flow are complex and tachyphylaxis to the ocular hypotensive effect develops fairly rapidly.

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Lesions of the serotonergic system impair the facilitation of but not the tolerance to the effects of chronic clenbuterol administration

et al. 1987

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Acute clenbuterol, a beta-adrenergic stimulant, decreases motility and antagonizes reserpine-induced hypothermia in mice. After repeated treatment with clenbuterol, the hypomotility disappears (tolerance) but the antagonism of reserpine-induced hypothermia increases (facilitation). To investigate the function of serotonin in tolerance and facilitation, lesions of the serotonergic system were performed by intracerebroventricular administration of the neurotoxin 5,7 dihydroxytryptamine (5,7-DHT). After lesions of the serotonergic system, the tolerance to clenbuterol-induced hypomotility persists, but the facilitation of the antagonism by clenbuterol of reserpine-induced hypothermia disappears. Thus, the serotonergic nerve terminals must be intact for the latter but not the former response to occur. Since the reversal of reserpine-induced hypothermia in animals is predictive of antidepressant effects in man, it is suggested that the therapeutic action of clenbuterol in depressed patients may be mediated through the serotonergic system.

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Tolerance to or facilitation of pharmacological effects induced by chronic treatment with the beta-adrenergic stimulant clenbuterol

Cited by 10 publications

References 30 publications

Myotoxic effects of clenbuterol in the rat heart and soleus muscle

Myotoxic effects of clenbuterol in the rat heart and soleus muscle

Effects of Ibuterol, a β-2 Adrenergic Prodrug, on Intraocular Pressure

Lesions of the serotonergic system impair the facilitation of but not the tolerance to the effects of chronic clenbuterol administration

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