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Alpha 2-adrenergic receptors mediate the increase in blood glucose levels induced by epinephrine and brief footshock stress.

Author information

1
Department of Psychology, Carleton University, Ottawa, Ontario, Canada.

Abstract

1. The purpose of the present experiments was to determine which adrenergic receptor(s) mediated the blood glucose surge following administration of epinephrine and brief footshock stress. 2. It was found that the order of potency of adrenergic agonists to increase blood glucose levels was: clonidine (alpha 2) much greater than epinephrine (alpha + beta) much greater than isoproterenol (beta) greater than phenylephrine (alpha 1). 3. The blood glucose increases caused by both epinephrine and footshock stress were greatly attenuated by the alpha-adrenergic antagonist, phentolamine (1.0 and 5.0 mg/kg ip), while the beta-adrenergic antagonist, propranolol (1.0 or 5.0 mg/kg ip), was without effect. Furthermore, it was found that the alpha 2-adrenergic antagonist, yohimbine (5.0 mg/kg ip), attenuated the epinephrine-induced increase in blood glucose levels, whereas the alpha 1 antagonist, phenoxybenzamine (5.0 mg/kg ip) dramatically potentiated the rise in glucose levels. 4. We conclude that the increase in blood glucose levels following brief footshock stress or injection of epinephrine is mediated by alpha 2-adrenergic receptors.

PMID:
2838868
DOI:
10.1016/0278-5846(88)90049-8
[Indexed for MEDLINE]

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