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Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin

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Abstract

Amitraz (N′-[2,4-dimethylphenyl]-N-[(2,4-dimethylphenyl)imino]-N-methylmethanimidamide) is a formamidine insecticide/acaricide that increases plasma glucose and decreases plasma insulin concentrations in dogs when applied topically. Because amitraz activates α2-adrenoceptors in numerous tissues, in this study we used rats as a model to determine whether these effects of amitraz are mediated by α2-adrenoceptors. The i. v. injection of amitraz (0.1, 0.3, and 1 mg/kg) followed by i.v. glucose injection (1 g/kg) induced a dose-dependent glucose intolerance characterized by hypoinsulinemia. At 1 mg/kg, amitraz completely blocked the insulin release induced by i. v. glucose administration. The α2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.) prevented the effects of amitraz, but the α1-adrenoceptor antagonist prazosin (0.3 mg/kg, i.v.) did not. The results suggested that one mechanism by which amitraz prolongs glucose-induced hyperglycemia is via inhibition of insulin release and this effect is mediated by α2-adrenoceptors.

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Authors and Affiliations

  1. Department of Veterinary Physiology and Pharmacology, Iowa State University, 50011, Ames, IA, USA

    Brent E. Smith & Walter H. Hsu

  2. Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, 50011, Ames, IA, USA

    Ping-Cheng Yang

Authors
  1. Brent E. Smith
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  2. Walter H. Hsu
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  3. Ping-Cheng Yang
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Smith, B.E., Hsu, W.H. & Yang, PC. Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin. Arch Toxicol 64, 680–683 (1990). https://doi.org/10.1007/BF01974698

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  • DOI: https://doi.org/10.1007/BF01974698

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