Moxonidine and rilmenidine injected into the medial septal area reduces the salivation induced by pilocarpine (original) (raw)
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Moxonidine reduces pilocarpine-induced salivation in rats
Autonomic Neuroscience-basic & Clinical, 2001
Cholinergic agonists activate salivation and the a -adrenergic and imidazoline receptor agonists induce opposite effects. In the present 2 Ž . Ž . Ž study, we investigated the effects of intracerebroventricular i.c.v. or intraperitoneal i.p. injection of moxonidine an a -adrenergic and 2 2
Inhibition of pilocarpine-induced salivation in rats by central noradrenaline
Archives of oral …, 2002
Peripheral treatment with cholinergic or adrenergic agonists results in salivation and the possibility of synergy between cholinergic and adrenergic efferent mechanisms in the control of salivation has been proposed. Central injections of the cholinergic agonist pilocarpine also induce salivation, while the effects of central injections of noradrenaline (norepinephrine) are not known. Here (a) the effects of intracerebroventricular (icv) injection of noradrenaline on the salivation induced by icv or intraperitoneal (i.p.) injection of pilocarpine and (b) the receptors involved in the effects of central noradrenaline on pilocarpine-induced salivation were investigated. Male Holtzman rats with a stainless-steel guide cannula implanted into the lateral ventricle were used. Rats were anaesthetized with tribromoethanol (200 mg/kg body weight) and saliva was collected on small, preweighed cotton balls inserted into the animal’s mouth. Noradrenaline (40, 80 and 160 nmol/1 μl) injected icv reduced the salivary secretion induced by pilocarpine (0.5 μmol/1 μl) injected icv. Noradrenaline (80 and 160 nmol/1 μl) injected icv also reduced the salivation induced by pilocarpine (4 μmol/kg) injected i.p. Previous treatment with the α2-adrenergic receptor antagonists RX 821002 (40, 80 and 160 nmol/1 μl) or yohimbine (160 and 320 nmol/1 μl) abolished the inhibitory effect produced by icv injection of noradrenaline on pilocarpine-induced salivation in rats. Prazosin (α1-adrenergic receptor antagonist) injected icv did not change the effect of noradrenaline on pilocarpine-induced salivation. Prior icv injection of only RX 821002 (80 or 160 nmol/1 μl) or yohimbine (320 nmol/1 μl) increased pilocarpine-induced salivation. The results show that (1) contrary to its peripheral effects, noradrenaline acting centrally inhibits cholinergic-induced salivation in rats; (2) central mechanisms involving α2-adrenergic receptors inhibit pilocarpine-induced salivation.
Life Sciences, 2002
Our studies have focused on the effect of injection of L-NAME and sodium nitroprussiate (SNP) on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine which was injected into the medial septal area (MSA). Rats were anesthetized with urethane (1.25 g/kg b. wt.) and a stainless steel cannula was implanted into their MSA. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into MSA. Injection of pilocarpine (10, 20, 40, 80, 160 mg/ml) into MSA produced a dose-dependent increase in salivary secretion. L-NG-nitro arginine methyl-esther (L-NAME) (40 mg/ml), a nitric oxide (NO) synthase inhibitor, was injected into MSA prior to the injection of pilocarpine into MSA, producing an increase in salivary secretion due to the effect of pilocarpine. Sodium nitroprussiate (SNP) (30 mg/ml) was injected into MSA prior to the injection of pilocarpine into MSA attenuating the increase in salivary secretion induced by pilocarpine. Medial arterial pressure (MAP) increase after injections of 0024-3205/02/$ -see front matter D 2002 Elsevier Science Inc. All rights reserved. PII: S 0 0 2 4 -3 2 0 5 ( 0 2 ) 0 1 5 3 1 -X (W.A. Saad).
Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine
Brain research, 2003
Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the α2-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 μmol/kg of body weight) i.p. reduced SSG vascular resistance (−50±13% vs. vehicle: 5±3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15±5% vs. vehicle: 2±3%) and MAP (16±3 mmHg, vs. vehicle: 2±3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88±12% vs. vehicle: 7±4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine.
Life Sciences, 2004
Male Holtzman rats weighting 200 -250 g were anesthetized with zoletil 50 mg/Kg (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle and stainless steel cannulas were implanted into their supraoptic nucleus (SON). We investigated the effects of the injection into the supraoptic nucleus (SON) of FK 409, a nitric oxide donor, and N W -nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor (NOS), on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine, which was injected into SON. The drugs were injected in 0.5 Al volume over 30-60 s. Controls was injected with a similar volume of 0.15 M NaCl. FK 409 and L-NAME were injected at doses of 20 Ag/0.5 Al and 40 Ag/0.5 Al respectively. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into SON. Injection of pilocarpine (10, 20, 40, 80, 160 Ag/Al) into SON produced a dose-dependent increase in salivary secretion. L-NAME was injected into SON prior to the injection of pilocarpine into SON, producing an increase in salivary secretion due to the effect of pilocarpine. FK 409 injected into SON attenuating the increase in salivary secretion induced by pilocarpine. Mean arterial pressure (MAP) increase after injections of pilocarpine into the SON. L-NAME injected into the SON prior to injection of pilocarpine into SON increased the 0024-3205/$ -see front matter D (W.A. Saad). www.elsevier.com/locate/lifescie Life Sciences 74 (2004) 1593 -1603
Effect of CP-96,345, a nonpeptide substance P receptor antagonist, on salivation in rats
Proceedings of the National Academy of Sciences, 1991
CP-96,345 [(2S,3S)-cis-2-(diphenylmethyl)-N-[(2-methoxyphenyl) methyl]-1-azabicyclo[2.2.2]octan-3-amine) antagonism of substance P-stimulated salivation was investigated in pentobarbital-anesthetized rats. Administered either intraperitoneally or orally, CP-96,345 produced dose-dependent inhibition of the sialogogic response elicited by substance P, with a median effective dose of 12-24 mumol/kg (5-10 mg/kg) of body weight, but had no effect on acetylcholine-stimulated salivation. CP-96,345 produced concentration-dependent inhibition of [3H]substance P binding to rat submaxillary gland membranes, with a median effective concentration of 34 +/- 3.6 nM. These biological activities were confined to CP-96,345 in that the 2R,3R enantiomer (CP-96,344) was without effect.