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Luca Pani - One of the best experts on this subject based on the ideXlab platform.
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Ritanserin counteracts both rat vacuous chewing movements and nigro striatal tyrosine hydroxylase immunostaining alterations induced by haloperidol
European Journal of Pharmacology, 2004Co-Authors: Giorgio Marchese, Francesco Bartholini, Stefania Ruiu, Paola Casti, Gian Luca Casu, Luca PaniAbstract:The effect of subchronic co-administration of Ritanserin (1.5 mg/kg, i.p., twice a day) and haloperidol (1 mg/kg, i.p., twice a day) on rat vacuous chewing movements and on tyrosine hydroxylase-immunostaining was investigated. Ritanserin significantly reduced rat vacuous chewing movements observed following 2, 3 and 4 weeks of haloperidol administration and after 5 days of haloperidol withdrawal. Furthermore, Ritanserin prevented the reduction of striatal tyrosine hydroxylase-immunostaining and the shrinkage of nigral dopaminergic cell bodies induced by haloperidol. The present results indicate that Ritanserin may possess protective properties on both dopaminergic nigro-striatal neuron alterations and vacuous chewing movements induced by haloperidol, and provide further evidence indicating a possible association between these two haloperidol-induced effects.
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the 5 ht2 antagonist Ritanserin blocks dopamine re uptake in the rat frontal cortex
Molecular Psychiatry, 2000Co-Authors: Stefania Ruiu, Giorgio Marchese, Luca Pani, Pierluigi Saba, Gian Luigi GessaAbstract:The effect of Ritanserin on dopamine (DA) re-uptake and efflux was studied in rat frontal cortex synaptosomes. When compared to other 5HT2 receptor antagonists such as ketanserin and risperidone or DA D2 receptor antagonists such as haloperidol and raclopride, the effect of Ritanserin proved to be more potent. Ritanserin blocked the DA transporter with a Ki of 0.18 +/- 0.06 microM, similar to cocaine (0.11 +/- 0.005 microM), while ketanserin had a Ki of 0.93 +/- 0.045; haloperidol of 2.07 +/- 0.12; risperidone of 18.01 +/- 0.62 and raclopride of 24.01 +/- 1.55. In addition, 15 min from its local application to the synaptosomes, Ritanserin potently released [3]H-DA leaving only 29.6 +/- 1.6% of DA content, while ketanserin effect was equal to 46.5 +/- 0.9%; haloperidol to 70.4 +/- 2.2% and risperidone to 73.9 +/- 1.5%, all tested at the dose of 10 microM. Cocaine had no effect on DA efflux. These results suggest that Ritanserin has a intrinsic dopaminergic effect which may help to explain its reported improvement on mood, cognition and negative symptoms of schizophrenia.
Joan Rodés - One of the best experts on this subject based on the ideXlab platform.
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Effects of Ritanserin, a selective and specific S2-serotonergic antagonist, on portal pressure and splanchnic hemodynamics in rats with long-term bile duct ligation
Hepatology (Baltimore Md.), 1993Co-Authors: Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Juan Carlos García-pagán, Faust Feu, Isabel Cirera, Joan RodésAbstract:This study investigated the short-term effects of Ritanserin, a selective and specific S2-serotonergic antagonist, in an experimental model of cirrhosis and intrahepatic portal hypertension caused by long-term bile duct ligation and division and in normal control rats. The rats subjected to bile duct ligation were randomized under blind conditions into two groups to receive Ritanserin (0.7 mg/kg body wt, intravenously; n = 10) or the same volume of placebo (isotonic saline solution; n = 10). We performed hemodynamic studies with radiolabeled microspheres 60 min after drug administration. Two groups of normal rats (n = 6) were studied after they received Ritanserin or placebo. Ritanserin administration to rats subjected to bile duct ligation significantly reduced portal pressure (from 16.2 ± 1.3 mm Hg to 12.3 ± 0.7 mm Hg; mean decrease, 22% ± 5%; p < 0.05). This reduction was associated with lower portal venous resistance (4.3 ± 0.5 mm Hg ± min. 100 gm/ml in the placebo group vs. 3.1 ± 0.3 mm Hg. min. 100 gm/ml in rats given Ritanserin; mean decrease, 28%; p = 0.069), but we saw no changes in portal vein inflow (3.9 ± 0.5 ml/min ± 100 gm vs. 4.4 ± 0.4 ml/min ± 100 gm), mean arterial pressure (110 ± 9 mm Hg vs. 102 ± 9 mm Hg) and cardiac index (32.9 ± 2.7 ml/min ± 100 gm vs. 40.5 ± 6.7 ml/min ± 100 gm). Hepatic arterial and kidney blood flows were not modified by Ritanserin. Ritanserin had no systemic or splanchnic effects in normal rats. Our results demonstrate that Ritanserin infusion decreases portal pressure without any systemic hemodynamic change in rats with secondary biliary cirrhosis and portal hypertension. These findings provide further support for a role of serotonin in the pathogenesis of portal hypertension and suggest a potential use of Ritanserin (alone or associated with other agents) in the pharmacological treatment of portal hypertension. (HEPATOLOGY 1993;18:389–393).
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effects of Ritanserin a selective and specific s2 serotonergic antagonist on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology, 1991Co-Authors: Frederik Nevens, Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of Ritanserin, a selective S2-serotonergic antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received Ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the Ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by Ritanserin. In summary, our results demonstrate that Ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
Maurizio Massi - One of the best experts on this subject based on the ideXlab platform.
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the nucleus accumbens is a site of action for the inhibitory effect of Ritanserin on ethanol intake in rats
Pharmacology Biochemistry and Behavior, 1993Co-Authors: Izabela Panocka, Roberto Ciccocioppo, Polidori Carlo, Maurizio MassiAbstract:Abstract The present study evaluated the effect of central injections of the 5-HT 2/1C receptor antagonist, Ritanserin, on ethanol intake in rats with developed preference for 3% ethanol. Intracerebroventricular (ICV) injections of Ritanserin (10 μg/rat/day for 10 days) decreased ethanol preference, while subcutaneous (SC) treatment with the same dose was ineffective. Ritanserin ICV, 1 μg/rat/day, did not reduce alcohol preference. Bilateral injections of Ritanserin into the nucleus accumbens (NAC; 0.5 μg/ site/day for 10 days) produced a prompt and very pronounced suppression of ethanol preference, without affecting total fluid intake. Bilateral injections of Ritanserin (0.5 μg/site/day for 10 days) into the ventral tegmental area (VTA) or into the medial prefrontal cortex (MPC) evoked only slight and variable reduction of ethanol preference. Injections of Ritanserin, 5 μg/site/day, into the VTA gave a nonselective suppression of the ingestive behavior. The present results provide evidence for a central site of action for the effect of Ritanserin on ethanol intake and suggest that the NAC might be a highly sensitive site for its action. Since the NAC is a major target of the mesolimbic dopaminergic system, they also suggest that the effect of Ritanserin might be due to interference with this system.
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long lasting suppression of alcohol preference in rats following serotonin receptor blockade by Ritanserin
Brain Research Bulletin, 1992Co-Authors: Izabela Panocka, Maurizio MassiAbstract:Abstract Rats with developed preference for 3% ethanol were injected subcutaneously (SC) with 10 mg/kg of the 5HT2 antagonist Ritanserin for 9 days. This resulted in a marked and significant suppression of alcohol preference, as compared to controls. The effect was very long-lasting, as shown by the fact that it was still evident up to 20 days after the end of the treatment. Since Ritanserin shows some affinity also for D2-dopaminergic receptors (even though much lower than for 5HT2 receptors), for comparison, other rats were injected SC for 9 days with 0.0625 mg/kg of haloperidol or with its vehicle. The effect of haloperidol treatment was low and short-lasting. Depletion of endogenous serotonin by p-chlorophenylalanine (600 mg/kg × 3 days) completely abolished the suppression of alcohol preference by Ritanserin. These results suggest that: 1) the Ritanserin-induced reduction of alcohol preference is not due to dopaminergic blockade, 2) that the effect of Ritanserin is completely dependent on the endogenous serotoninergic mechanisms.
P J Cowen - One of the best experts on this subject based on the ideXlab platform.
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Ritanserin attenuates anorectic endocrine and thermic responses to d fenfluramine in human volunteers
Psychopharmacology, 1993Co-Authors: E M Goodall, P J Cowen, M Franklin, T SilverstoneAbstract:This study investigated the role of the 5-HT2/1C receptor antagonist Ritanserin ond-fenfluramine (d-FF) induced changes in food intake, prolactin (PRL) secretion and oral temperature in 12 healthy male volunteers. The study was double blind and placebo controlled. Food intake was measured using an automated food dispenser.d-FF (30 mg) significantly reduced fat intake. While Ritanserin (5 mg) had no effect when given alone it abolished thed-FF induced reduction in fat intake. In addition, Ritanserin abolished thed-FF induced rise in PRL and oral temperature. The results suggest that 5-HT2 or 5-HT1C receptors mediate the effects ofd-fenfluramine on appetite, prolactin secretion and temperature in humans.
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slow wave sleep and 5 ht2 receptor sensitivity in generalised anxiety disorder a pilot study with Ritanserin
Psychopharmacology, 1992Co-Authors: J M Da Roza Davis, A L Sharpley, P J CowenAbstract:Eight patients with generalised anxiety disorder (GAD) and eight matched healthy controls had their polysomnogram measured on two occasions separated by 1 week. On one occasion they received the 5-HT2 receptor antagonist, Ritanserin (5 mg orally) and on the other matching placebo. The increase in slow wave sleep produced by Ritanserin was the same in GAD patients as in healthy controls. These findings do not support the hypothesis that GAD is associated with a generalised hypersensitivity of brain 5-HT2 receptors; however, the present data cannot exclude the presence of a regionally specific change in this receptor subtype in anxiety disorders.
W D Dietrich - One of the best experts on this subject based on the ideXlab platform.
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the effect of Ritanserin a 5 ht2 receptor antagonist on ischemic cerebral blood flow and infarct volume in rat middle cerebral artery occlusion
Stroke, 1994Co-Authors: Kiyoshi Takagi, Myron D Ginsberg, Mordecai Y T Globus, Raul Busto, W D DietrichAbstract:In a previous study from our laboratory, Ritanserin, a specific 5-HT2 serotonin receptor antagonist, reduced ischemic damage in the setting of transient global ischemia. In this study, we examined the effect of Ritanserin on ischemic cerebral blood flow, systemic blood pressure, and infarct volume in the model of permanent focal ischemia with brain temperature controlled at 35.0 degrees C to 36.0 degrees C. Thirty-seven male Sprague-Dawley rats were used. The right middle cerebral artery was permanently occluded. Ritanserin (8 mg/kg) or vehicle was continuously administered intravenously for 90 minutes starting 10 minutes after middle cerebral artery occlusion. Cerebral blood flow was monitored by laser Doppler flowmetry in the ischemic cortex before and for 2 hours after arterial occlusion. Brains were perfusion-fixed 3 days later, and infarct volumes were measured. Mean arterial blood pressure was not affected by treatment. In the vehicle and Ritanserin groups, mean ischemic cerebral blood flow (percent of preischemic values) was 34.6 +/- 14.7% (mean +/- SD) and 26.6 +/- 15.0%, respectively. Hemispheric infarct volumes were 119.3 +/- 49.4 mm3 and 136.6 +/- 49.6 mm3, respectively. No significant differences were recognized. Intravenous administration of Ritanserin did not affect mean arterial blood pressure or cerebral blood flow in the ischemic region during the acute phase of ischemia. No protective effect of Ritanserin was apparent in the setting of permanent focal ischemia when treatment was begun shortly after the onset of ischemia.
