Moxonidine reduces pilocarpine-induced salivation in rats

Moreira, Thiago S.; Takakura, Ana C.; Luca, Laurival A. De; Renzi, Antonio; Menani, José Vanderlei

doi:10.1016/s1566-0702(01)00296-x

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…With atropine methyl bromide, it was possible to block the access of systemic pilocarpine to brain muscarinic receptors and inhibit salivation stimulated by pilocarpine. These results are consistent with disruption of peripheral pilocarpine-induced salivation by focal cerebral lesions or central ␣ 2 -adrenoceptor activation (Renzi et al, 1993;Moreira et al, 2001;Renzi et al, 2002), and with the peripheral and central effects of another cholinergic agonist, oxotremorine, on salivation (Sanchez and Meier, 1993). One difference from previous data on oxotremorine (Sanchez and Meier, 1993) is that, with 4 mol/kg of pilocarpine, we did not detect tremors or other signs of seizures in the awake animal (unpublished results).…”

Section: Discussionsupporting

confidence: 89%

“…Pilocarpine injected into the lateral cerebral ventricles also induces salivation, an action that seems dependent on activation of sympathetic efferent fibers (Cecanho et al, 1999). Finally, pilocarpine-induced salivation is reduced by central, but not peripheral, injections of the antihypertensive agent moxonidine (Moreira et al, 2001). These findings are all consistent with the ability of pilocarpine to cross the blood-brain barrier (Freedman et al, 1989).…”

Section: Introductionmentioning

confidence: 55%

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Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

et al. 2003

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Although cholinergic agonists such as pilocarpine injected peripherally can act directly on salivary glands to induce salivation, it is possible that their action in the brain may contribute to salivation. To investigate if the action in the brain is important to salivation, we injected pilocarpine intraperitoneally after blockade of central cholinergic receptors with atropine methyl bromide (atropine-mb). In male Holtzman rats with stainless steel cannulas implanted into the lateral ventricle and anesthetized with ketamine, atropine-mb (8 and 16 nmol) intracerebroventricularly reduced the salivation induced by pilocarpine (4 micro mol/kg) intraperitoneally (133 + 42 and 108 + 22 mg/7 min, respectively, vs. saline, 463 + 26 mg/7 min), but did not modify peripheral cardiovascular responses to intravenous acetylcholine. Similar doses of atropine-mb intraperitoneally also reduced pilocarpine-induced salivation. Therefore, systemically injected pilocarpine also enters the brain and acts on central muscarinic receptors, activating autonomic efferent fibers to induce salivation.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 55%

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

et al. 2003

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“…Although pilocarpine-induced salivation is suggested to depend on activation of central mechanisms (Moreira et al, 2001(Moreira et al, , 2002Takakura et al, 2003Takakura et al, , 2009Borella et al, 2008), similar to a previous study (Inenaga et al, 2008) no increase in the number of c-fos immunoreactive cells in the salivary nuclei of the brainstem was found in the present study (data not shown). In addition, we found no evidence in the literature suggesting that peripheral pilocarpineinduced salivation involves the activation of the salivary nuclei in the brainstem.…”

Section: Discussionsupporting

confidence: 90%

Central mechanisms involved in pilocarpine-induced pressor response

Takakura

Moreira

Borella

et al. 2011

Autonomic Neuroscience

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Pilocarpine (cholinergic muscarinic agonist) injected peripherally may act centrally to produce pressor responses; in the present study, using c-fos immunoreactive expression, we investigated the forebrain and brainstem areas activated by pressor doses of intravenous (i.v.) pilocarpine. In addition, the importance of vasopressin secretion and/or sympathetic activation and the effects of lesions in the anteroventral third ventricle (AV3V) region in awake rats were also investigated. In male Holtzman rats, pilocarpine (0.04 to 4μmol/kg b.w.) i.v. induced transitory hypotension followed by long lasting hypertension. Sympathetic blockade with prazosin (1mg/kg b.w.) i.v. or AV3V lesions (1 day) almost abolished the pressor response to i.v. pilocarpine (2μmol/kg b.w.), whereas the vasopressin antagonist (10μg/kg b.w.) i.v. reduced the response to pilocarpine. Pilocarpine (2 and 4μmol/kg b.w.) i.v. increased the number of c-fos immunoreactive cells in the subfornical organ, paraventricular and supraoptic nuclei of the hypothalamus, organ vasculosum of the lamina terminalis, median preoptic nucleus, nucleus of the solitary tract and caudal and rostral ventrolateral medulla. These data suggest that i.v. pilocarpine activates specific forebrain and brainstem mechanisms increasing sympathetic activity and vasopressin secretion to induce pressor response.

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“…Salivation is controlled by the autonomic nervous system not only by direct activation of salivary gland receptors but also by activation of brain mechanisms (36)(37)(38)(39). Moreover, it has been reported that atropine, a muscarinic antagonist, injected intracerebroventricularly reduced the salivation induced by pilocarpine, a muscarinic agonist, injected ip, suggesting that pilocarpine enters the brain and acts on central muscarinic receptors, activating autonomic efferents to induce salivation (37).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Salivary Secretion by Activation of Cannabinoid Receptors

Prestifilippo

Fernández‐Solari

Cal

et al. 2006

Exp Biol Med (Maywood)

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It is known that marijuana use decreases saliva secretion. Therefore, we hypothesized that cannabinoid receptors (CBs) are located in salivary glands to mediate that effect. In these experiments, we used the submandibular gland (SMG) of male rats, which is one of the major salivary glands. Mammalian tissues contain at least two types of CBs, CB1 and CB2, mainly located in the nervous system and peripheral tissues, respectively. Both receptors are coupled to Gi protein and respond by inhibiting the activity of adenylyl cyclase. We demonstrated that both CB1 and CB2 are present in the SMG, each showing specific localizations. The best-known endocannabinoid is anandamide (AEA), which binds with high affinity to CB1 and CB2. We showed that AEA markedly reduced forskolin-induced increase of cAMP content in vitro. This effect was blocked by AM251 and AM630 (CB1 and CB2 antagonists, respectively), indicating that both receptors are implicated in SMG physiology. In addition, we showed that AEA injected intraglandularly to anesthetized rats inhibited norepinephrine (NE)- and methacholine (MC)-stimulated saliva secretion in vivo and that both AM251 or AM630 prevented the inhibitory action of AEA. Also, the intraglandular injection of AM251 increased saliva secretion induced by lower doses of NE or MC. This increase was synergized after coinjection with AM630. Therefore, we concluded that AEA decreases saliva secretion in the SMG acting through CB1 and CB2 receptors.

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Moxonidine reduces pilocarpine-induced salivation in rats

Cited by 11 publications

References 20 publications

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Central mechanisms involved in pilocarpine-induced pressor response

Inhibition of Salivary Secretion by Activation of Cannabinoid Receptors

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