Clonidine inhibits salivary secretion by activation of postsynaptic ?2-receptors

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Abstract
The effects of clonidine on the submaxillary gland of the rat were studied. Doses ranging between 100 to 3.000 μg/kg produced a sustained secretory response which was blocked by 0.1 mg/kg of prazosin but not by 1 mg/kg of yohimbine. Clonidine 10 μg/kg markedly inhibited the salivation induced by noradrenaline, methacholine and substance P but not that induced by isoproterenol. The inhibition caused by the α2-agonist was greater for noradrenaline than for either methacholine or substance P. Blockade of α2 adrenoceptors with yohimbine (0.3–1 mg/kg) prevented the inhibition by clonidine of noradrenaline, methacholine and substance P induced salivation. On the other hand, prazosin 0.1 mg/kg did not modify the inhibition by clonidine of methacholine induced secretion. The results obtained indicate that clonidine exerts a dual effect on salivary secretion: at high doses it elicits salivation through activation of α1-adrenoreceptors; at the dose of 10 μg/kg clonidine activates α2-adrenoreceptors which inhibit the secretory response evoked through either muscarine, substance P and α1-adrenorecptors agonists.