POSTSYNAPTIC ALPHA-2 ADRENERGIC-RECEPTORS IN ISOLATED RAT ISLETS OF LANGERHANS - INHIBITION OF INSULIN RELEASE AND CYCLIC 3'-5'-ADENOSINE MONOPHOSPHATE ACCUMULATION

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Abstract
Effects of various .alpha.-adrenergic agents on insulin release and cAMP accumulation in pancreatic islets were investigated. Clonidine, epinephrine, .alpha.-methylnorepinephrine and norepinephrine were most potent, and methoxamine and phenylephrine least potent in inhibiting the glucose-stimulated insulin release. Yohimbine and phentolamine were the most effective, and prazosin was the least effective in antagonizing the epinephrine-inhibited insulin release. Clonidine markedly inhibited the glucagon-stimulated cAMP accumulation, whereas methoxamine showed weak inhibition. Yohimbine markedly increased cAMP accumulation in the presence of epinephrine, but prazosin showed little effect. The effects of .alpha.-adrenergic agents on rabbit aorta contraction were also examined for comparison with .alpha.-adrenergic receptors in pancreatic islets. In the aorta, the order of agonist potency was norepinephrine > phenylephrine > epinephrine > methoxamine > .alpha.-methylnorepinephrine, and that of antagonist potency was prazosin > WB-4101 [2-N-2,6-dimethoxyphenoxyethylamino methyl-1,4-benzodioxane] > phentolamine > dihydroergotamine > phenoxybenzamine > yohimbine. These orders of potencies were markedly different from those in pancreatic islets. The .alpha. adrenergic receptors in rat pancreatic islets are different from those on rabbit aorta (.alpha.-1), and are typical postsynaptic .alpha.-2 adrenergic receptors.