Effects of α1- and α2-Adrenoceptor Stimulation and Blockade on Plasma Insulin Levels in the Mouse

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Abstract
Stimulation of alpha-adrenoceptors is known to inhibit insulin secretion under a variety of conditions. In this study, the question of whether these alpha-adrenoceptors are of the alpha 1- or the alpha 2-subtype was investigated in the mouse. The selective alpha 2-adrenoceptor agonist clonidine (0.05-50 nmol/kg) was found to markedly inhibit the insulin secretory response to both glucose and the cholinergic agonist carbachol. This inhibition of insulin secretion was counteracted by the alpha 2-adrenoceptor antagonist yohimbine (2.6 mumol/kg), but not by the alpha 1-adrenoceptor antagonist prazosin (2.6 mumol/kg). In contrast, the alpha 1-adrenoceptor agonist phenylephrine (0.05-50 nmol/kg) did not affect the insulin secretory response to either glucose or carbachol. Moreover, both yohimbine and prazosin increased basal plasma insulin levels. It is concluded that alpha 1- and alpha 2-adrenoceptor blockade is followed by enhancement of basal plasma insulin levels in the mouse, whereas alpha 2-adrenoceptor stimulation but not alpha 1-adrenoceptor stimulation impairs the insulin secretory response to glucose and carbachol.

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