Stimulation of parotid cell glucose oxidation. Role of alpha 1-adrenergic receptors and calcium mobilization.
Epinephrine stimulated glucose oxidation in isolated rat parotid cell aggregates through alpha- and beta-adrenergic mechanisms. The alpha-adrenergic component appeared to be of the alpha 1-receptor subtype as evidenced by inhibition studies with selective antagonists. Calcium mobilization in the presence of the ionophore A23187 was as capable as epinephrine in eliciting this response. Epinephrine stimulation of glucose oxidation was, however, only partially dependent on extracellular calcium. Only the upper 50% of the maximal (10(-5) M) epinephrine response required external calcium, since stimulation by 10(-6) M epinephrine, which elicits only about 40% of the maximal (10(-5) M epinephrine) response, was independent of external calcium. Furthermore, no external calcium dependence was observed for pure alpha- or beta-adrenergic stimulation alone, which comprised about 60 and 40%, respectively, of the maximal epinephrine response. Thus, adrenergic mediated parotid cell glucose oxidation may proceed by different mechanisms depending on the extent and nature of cellular stimulation.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D008297:Male; D010306:Parotid Gland / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D011942:Receptors, Adrenergic, alpha; D000001:Calcimycin; D004533:Egtazic Acid; D005947:Glucose; D002118:Calcium; D004837:Epinephrine