Alpha-2 adrenoreceptors mediate clonidine-induced hypoinsulinaemia in sheep. 
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 micrograms/kg or 5 micrograms/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 micrograms/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.