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Down-regulation of beta-adrenergic receptors and up-regulation of estrogen and progesterone receptors induced in the reproductive system of female veal calves by dietary clenbuterol


Down-regulation of beta-adrenergic receptors and up-regulation of estrogen and progesterone receptors induced in the reproductive system of female veal calves by dietary clenbuterol



American Journal of Veterinary Research 56(11): 1493-1497



ISSN/ISBN: 0002-9645

PMID: 8585662

Effects induced by long-term administration of clenbuterol at anabolic dosages (20 micrograms/kg of body weight for 40 days) on beta-adrenergic receptor (beta-AR) subtypes, estrogen receptors (ER), and progesterone receptors (PgR) in the reproductive system of female veal calves were investigated. Clenbuterol treatment induced a significant (P < 0.01) down-regulation of beta-AR subtypes (beta 1-AR, beta 2-AR, myometrial high-affinity beta 2-AR, and ovarian low-affinity beta 2-AR). On the other hand, a significant (P < 0.01) increase of uterine and ovarian ER and PgR receptors was observed in treated calves. Treatment did not affect dissociation constant values of beta-AR, ER, or PgR. In similar manner, clenbuterol did not significantly modify distribution of ER and PgR in the various tissues of the genital tract. In fact, these receptors were significantly (P < 0.05) more concentrated in the uterus than in the vagina in treated and untreated calves. Data indicated that prolonged clenbuterol exposure induced homologous beta-AR down-regulation (down-regulation of its specific receptors) and heterologous ER and PgR up-regulation (up-regulation of different types of receptors, not specifically bound by clenbuterol) in the genital tract of veal calves. Modification of the receptorial status could be reasonably related to the pathologic changes observed in long-term treated calves (eg, hydrometra, dilatation of uterine glands, cystic ovaries). The increased concentrations of ER and PgR suggested the possible existence of subcellular mechanisms regulated by repeated beta-adrenergic stimulation.

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Accession: 008502755

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