Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Abstract

1. In conscious fasted rabbits an intravenous infusion of clonidine (2 micrograms kg-1 min-1) induced hyperglycaemia. The increase in blood glucose was accompanied by an inhibition of insulin secretion and basal lipolysis. 2. Yohimbine infused at a rate of 20 micrograms kg-1 min-1 suppressed clonidine-induced hyperglycaemia and blocked the inhibitory effect on insulin secretion mediated by the alpha 2-adrenoceptor agonist. 3. The intravenous infusion of amidephrine (10 micrograms kg-1 min-1) induced an increase in insulin secretion in the absence of patent hyperglycaemia. Prazosin, 0.3 mg kg-1 s.c. selectively antagonized the effect of amidephrine on insulin secretion. 4. Isoprenaline infusion (4.4 micrograms kg-1 min-1) evoked a significant increase in blood glycerol and immunoreactive insulin plasma levels. Both responses were clearly attenuated when alpha 2-adrenoceptors were simultaneously stimulated by selective (clonidine) and less selective (phenylephrine, 20 micrograms kg-1 min-1) agonists. 5. Amidephrine infusion did not induce appreciable changes in blood glycerol nor did it modify, isoprenaline-induced lipolytic response. 6. Simultaneous infusion of isoprenaline and amidephrine induced a remarkable increase in insulin secretion. 7. It is concluded that in normal fasted rabbits stimulation of alpha 2-adrenoceptors depresses basal and beta-adrenoceptor mediated lipolysis and insulin secretion. On the other hand, selective stimulation of alpha 1-adrenoceptors does not affect lipolysis but induces insulin release. Simultaneous stimulation of alpha 1- and beta-adrenoceptors potentiates the insulin secretory response.