1 In conscious fasted rabbits an intravenous infusion of clonidine (2ygkg-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 20ogkg-min-' suppressed clonidine-induced hyperglycaemia and blocked the inhibitory effect on insulin secretion mediated by the a2-adrenoceptor agonist. 3 The intravenous infusion of amidephrine (10pgkg-'min-1) induced an increase in insulin secretion in the absence of patent hyperglycaemia. Prazosin, 0.3 mg kg1 s.c. selectively antagonized the effect of amidephrine on insulin secretion.4 Isoprenaline infusion (4.4 pgkg' min 1) evoked a significant increase in blood glycerol and immunoreactive insulin plasma levels. Both responses were clearly attenuated when a2-adrenoceptors were simultaneously stimulated by selective (clonidine) and less selective (phenylephrine, 20 yg kg-I min-') agonists. 5Amidephrine 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 oe2-adrenoceptors depresses basal and fl-adrenoceptor mediated lipolysis and insulin secretion. On the other hand, selective stimulation of a,-adrenoceptors does not affect lipolysis but induces insulin release. Simultaneous stimulation of a,-and fl-adrenoceptors potentiates the insulin secretory response.

1 In conscious fasted rabbits an intravenous infusion of phenylephrine (20 ptg kg-' min-) induced hyperglycaemia. The increase in blood glucose was accompanied by a modest increase in insulin secretion and a reduction of liver glycogen. Muscle glycogen and blood lactate levels were not altered by treatment with phenylephrine. 2 Prazosin, 1 mg kg-I s.c., partially attenuated phenylephrine-induced hyperglycaemia.3 Phenoxybenzamine infusion (16.6pgkg-'min-') for 15min suppressed the increase in blood glucose and the reduction in liver glycogen evoked by phenylephrine. This a-adrenoceptor blocker also clearly attenuated the blood glucose elevation observed on infusing adrenaline at 0.3 fig kg'-min -. 4 Blockade by phenoxybenzamine of phenylephrine-and adrenaline-induced hyperglycaemia was not accompanied by a significant increase in immunoreactive insulin plasma levels.5 Yohimbine infused at a rate of 20 g kg-lmin', also completely blocked phenylephrine-induced hyperglycaemia. This suppressor effect was accompanied by a marked rebound in insulin secretion. 6 It is concluded that in normal fasted rabbits stimulation of a-adrenoceptors induces hyperglycaemia. The increase in blood glucose depends mainly on liver glycogenolysis and inhibition of insulin secretion. Separate blockade of each component suffices to reduce a-adrenoceptor-mediated hyperglycaemia.

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