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Alpha‐2 adrenoreceptors mediate clonidine‐induced hypoinsulinaemia in sheep
Author(s) -
OSMAN T. E. A.,
NICHOLSON T.
Publication year - 1991
Publication title -
journal of veterinary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.527
H-Index - 60
eISSN - 1365-2885
pISSN - 0140-7783
DOI - 10.1111/j.1365-2885.1991.tb00839.x
Subject(s) - idazoxan , clonidine , prazosin , endocrinology , medicine , antagonist , alpha (finance) , alpha 2 adrenergic receptor , yohimbine , adrenergic receptor , chemistry , insulin , receptor , surgery , construct validity , patient satisfaction
Insulin and glucose concentrations in the blood of sheep were measured before, and up to 7 h after, feeding. The patterns reported by other workers were confirmed, namely: an early insulin concentration peak and decline in glucose concentration and, later, more prolonged changes. Intravenous injection of clonidine (2 μg/kg or 5 μg/kg) just before offering food caused hypoinsulinaemia and hyperglycaemia, abolishing the normal patterns. Administration of idazoxan (0.1 mg kg‐ 1 ), an alpha‐2 adrenoreceptor antagonist, before a 2 μg/kg dose of clonidine, completely blocked the effects of clonidine. By contrast, with prior injection of prazosin (0.1 mg/kg), an alpha‐1 adrenoreceptor antagonist, the hypoinsulinaemia in response to clonidine still occurred and the hyperglycaemia appeared to be enhanced. The antagonists injected alone had only slight effects: idazoxan caused a slight hypoglycaemia and prazosin a slight hyperglycaemia. The results indicate that clonidine causes hypoinsulinaemia and hyperglycaemia by action on alpha‐2 receptors. Possible mechanisms are discussed.