Adrenoceptor-Activation of Oxygen Consumption in Rat Parotid Acini

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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 .mu.M) 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 .mu.M) increased the O2 consumption with approximately 22%. Stimulation with the .alpha.-adrenergic agonist phenylephrine (10 .mu.M) 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.-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 apper is that only .beta.-and .alpha.i-adrenoceptors are functioning in the parotid acini and that phenylephrine acts as a partiel .alpha.i-agonist.