Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 45, Issue 9, Pages 1694-1699Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2007.03.002
Keywords
Clenbuterol; heart rate; Atenolol; ICI-118,551; growth promoters
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beta(2)-Receptor adrenergic agonists as clenbuterol and analogues are illegally used as growth promoters in cattle, in Europe, as well as in other countries. Following consumption of meat or liver, intoxication cases were described, and cardiovascular toxic effects (tachycardia, hypertension) were of clinical relevance. Therefore, we investigated whether heart rate increase induced by clenbuterol could depend upon stimulation of beta(1)- and/or beta(2)-adrenergic receptors, and in which ratio. We used in vitro guinea-pig atria, a model in which beta(1)-/beta(2)-receptors ratio is similar to that found in men. In our experiments both beta(1)- and beta(2)-receptors contributed to clenbuterol-induced heart rate increase, but with a different potency. The selective beta(2)-antagonist ICI- 118,551 competitively antagonized responses to clenbuterol with high affinity (pA(2) = 9.47 +/- 0.28, SchildSlope 0.98 +/- 0.20 not significantly different from unity, K-B 0.34 nM). The selective beta(1)-antagonist atenolol antagonized clenbuterol with a relatively lower affinity (pA2 = 7.59 +/- 0.14), the SchildSlope = 1.97 +/- 0.33 was significantly different from unity (P < 0.05). Results show that clenbuterol stimulates guinea-pig heart rate by acting chiefly on beta(2)-adrenoceptor, although responses to clenbuterol apparently are mediated by an inter-play between both beta-adrenoceptors. Further experiments are necessary to understand which beta-adrenergic antagonists are of effectiveness to counteract cardiovascular effects in case of intoxication following clenbuterol, or other P-adrenergic stimulants. (c) 2007 Elsevier Ltd. All rights reserved.
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