1. In conscious fasted rabbits the
insulin secretory response induced by the
intravenous infusion of the alpha1-adrenoceptor agonist,
amidephrine (10 microg kg(-1) min(-1)) was blocked by the simultaneous administration of
clonidine (2 microg kg(-1) min(-1) i.v.). 2. The excitatory effect of
amidephrine (10 microg kg(-1) min(-1)) on insulin secretion was similarly suppressed by the concomitant infusion of the selective alpha2-adrenoceptor agonist
UK14304 (1 microg kg(-1) min(-1)). Both, the increase in
blood glucose and the inhibition of insulin secretion found with
UK14304 when infused alone were antagonized in rabbits previously treated with the very selective alpha2-adrenoceptor antagonist
2-methoxyidazoxan (1.5 microg kg(-1) min(-1)). 3. The combined administration of
amidephrine (3 microg kg(-1) min(-1)) and
isoprenaline (0.3 microg kg(-1) min(-1)) evoked a potentiated increase in
insulin plasma levels in the face of a weak hyperglycaemia, an established reduction in blood pressure and
tachycardia. 4. The potentiated
insulin secretory response derived from alpha1- and beta-
adrenoceptor stimulation was blunted by
clonidine administration. In its presence a sustained hyperglycaemic response was found. 5. The increase in plasma
lactate levels resulting from dual
adrenoceptor stimulation (
amidephrine: 10 microg kg(-1) min(-1) +
salbutamol: 0.3 microg kg(-1) min(-1)) was smaller than the expected should addition or potentiation occurred. 6. Our results point to a possible physiological role played by alpha2-adrenoceptors on insulin secretion, since their stimulation by the endogenous
catecholamines could lead to inhibition of
insulin release, masking any potentiated response that otherwise should have appeared from alpha1- and beta-
adrenoceptor stimulation.