Clonidine inhibits salivary secretion by activation of postsynaptic alpha 2-receptors
- PMID: 6207441
- DOI: 10.1007/BF00501435
Clonidine inhibits salivary secretion by activation of postsynaptic alpha 2-receptors
Abstract
The effects of clonidine on the submaxillary gland of the rat were studied. Doses ranging between 100 to 3.000 micrograms/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 micrograms/kg markedly inhibited the salivation induced by noradrenaline, methacholine and substance P but not that induced by isoproterenol. The inhibition caused by the alpha 2-agonist was greater for noradrenaline than for either methacholine or substance P. Blockade of alpha 2 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 alpha 1-adrenoceptors; at the dose of 10 micrograms/kg clonidine activates alpha 2-adrenoceptors which inhibit the secretory response evoked through either muscarine, substance P and alpha 1-adrenoceptor agonists.