Activation of central α2 -adrenoceptors mediates salivary gland vasoconstriction

Abstract Objective Peripheral treatment with the cholinergic agonist pilocarpine increases salivary gland blood flow and induces intense salivation that is reduced by the central injection of moxonidine (α2 -adrenoceptors/imidazoline agonist). In the present study, we investigated the effects of the...

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Veröffentlicht in:Archives of oral biology 2013-02, Vol.58 (2), p.167-173
Hauptverfasser: Moreira, Thiago S, Takakura, Ana C, Menani, José V, Colombari, Eduardo
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Sprache:eng
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Zusammenfassung:Abstract Objective Peripheral treatment with the cholinergic agonist pilocarpine increases salivary gland blood flow and induces intense salivation that is reduced by the central injection of moxonidine (α2 -adrenoceptors/imidazoline agonist). In the present study, we investigated the effects of the intracerebroventricular (i.c.v.) injection of pilocarpine alone or combined with moxonidine also injected i.c.v. On submandibular/sublingual gland (SSG) vascular resistance. In addition, the effects of these treatments on arterial pressure, heart rate and on mesenteric and hindlimb vascular resistance were also tested. Design Male Holtzman rats with stainless steel cannula implanted into lateral ventricle and anaesthetized with urethane + α-chloralose were used. Results Pilocarpine (500 nmol/1 μl) injected i.c.v. Reduced SSG vascular resistance and increased arterial pressure, heart rate and mesenteric vascular resistance. Contrary to pilocarpine alone, the combination of moxonidine (20 nmol/1 μl) and pilocarpine injected i.c.v. Increased SSG vascular resistance, an effect abolished by the pre-treatment with the α2 -adrenoceptor antagonist yohimbine (320 nmol/2 μl). The increase in arterial pressure, heart rate and mesenteric resistance was not modified by the combination of moxonidine and pilocarpine i.c.v. Conclusion These results suggest that the activation of central α2 -adrenoceptors may oppose to the effects of central cholinergic receptor activation in the SSG vascular resistance.
ISSN:0003-9969
1879-1506
DOI:10.1016/j.archoralbio.2012.06.017