Adrenoceptor-activation of oxygen consumption in rat parotid acini

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.