PubMed1987
Previous studies from our laboratory showed 1) that adenosine (1.65 microM), a substance released by tissues in energy-deficient states, stimulated glucagon secretion by activation of A2 purinergic receptors, and 2) that this effect was potentiated by a low substimulating concentration of epinephrine through activation of alpha-adrenergic receptors. The present work was undertaken to assess the subtype of alpha-adrenergic receptor involved in this potentiation. Therefore, we used adrenergic blockers and agonist drugs more specific for alpha 1- or alpha 2-adrenergic receptors. The potentiating effect of epinephrine (0.01 microM) on glucagon secretion induced by adenosine (1.65 microM) was not prevented by an alpha 1-adrenergic blocker, prazosine (6 microM), but was suppressed by an alpha 2-adrenergic blocker, yohimbine (0.6 microM). The implication of alpha 2-adrenergic receptors in the potentiating effect was confirmed by the use of selective alpha 1- or alpha 2-adrenergic agonist drugs. Indeed, clonidine (0.01 microM), an alpha 2-agonist, ineffective per se, potentiated, whereas phenylephrine (0.01 microM), an alpha 1-agonist, had no effect on glucagon secretion induced by adenosine. We conclude that the potentiation by epinephrine of adenosine-induced glucagon secretion is mediated by alpha 2-adrenergic receptor activation. A potentiation between the effects of A2 purinergic and alpha 2-adrenergic agonists may be of physiological relevance in stressful energy-deficient states, when an increase in glucagon secretion is necessary.