title: Adrenoceptor-activation of oxygen consumption in rat parotid acini.
abstract: The purpose of this study was to examine the effects of various adrenergic agonists and antagonists upon rat parotid oxygen consumption. The experiments were performed using collagenase-isolated acini, and the O2 consumption was determined using a Gilson Oxygraph 5/6 H with a Clark electrode. Stimulation with the alpha- and beta-adrenergic agonist adrenaline (10 microM) lead to a 65% increase in parotid O2 consumption in about 10 sec. Addition of adrenaline after preincubation with the beta-adrenergic antagonist propranolol or the alpha-adrenergic antagonist prazosin showed that about 2/3 of the adrenaline-induced O2 consumption originated in alpha-adrenergic activity, whereas the remaining 1/3 stemmed from beta-adrenergic activity. Correspondingly, it was found that stimulation by the beta-adrenergic agonist isoprenaline (10 microM) increased the O2 consumption with approximately 22%. Stimulation with the alpha-adrenergic agonist phenylephrine (10 microM) did however, only increase O2 consumption with 21%. This finding is probably not related to the existence of alpha-2-adrenoceptors stimulated by adrenaline and not by phenylephrine, since: (1) the adrenaline-induced response was unaffected by preincubation by pertussis toxin, (an activator of the Gi protein of the adenylate cyclase complex), and (2) the stimulating effect of clonidine (an alpha-2-adrenoceptor agonist) was inhibited by preincubation with prazosin, and (3) radioligand binding studies using [3H]-yohimbine was unsuccessful in demonstrating parotid alpha-2-adrenoceptors. Accordingly, a conclusion that accounts for the findings in this paper is that only beta- and alpha 1-adrenoceptors are functioning in the parotid acini and that phenylephrine acts as a partiel alpha 1-agonist.
authors.affiliation: Department of Oral Pathology, Royal Dental College, Copenhagen N, Denmark.
authors.forename: U
authors.initials: U
authors.lastname: Glenert
authors.forename: B
authors.initials: B
authors.lastname: Nauntofte
mesh_terms: D037361:Adenylate Cyclase Toxin; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D003000:Clonidine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D003012:Microbial Collagenase / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects*; D010306:Parotid Gland / Q000378:metabolism*; D037342:Pertussis Toxin; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic / Q000378:metabolism*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D037361:Adenylate Cyclase Toxin; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D011941:Receptors, Adrenergic; D010566:Virulence Factors, Bordetella; D010656:Phenylephrine; D015016:Yohimbine; D037342:Pertussis Toxin; D003012:Microbial Collagenase; D007545:Isoproterenol; D003000:Clonidine; D004837:Epinephrine