SEARCH · Search PubMed

Results for “Reserpine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

PubMed1998

Cytochemical localization of ouabain-sensitive, K+-dependent p-nitrophenylphosphatase activity in the choroid plexus of normal and reserpinized guinea pigs.

High doses of reserpine induce depletion of biogenic amines. The K-NPPase activity of choroid plexus was determined after one-shot reserpine administration using cerium-based cytochemistry. In normal untreated animals, reaction product was found on the microvilli of the choroidal epithelium but was almost undetectable 3 and 7 days after reserpinization. At 20 days after reserpinization, however, it was detectable. These findings suggested that reserpine decreased the choroidal Na,K-ATPase activity, and that catecholamines might be essential to maintain normal choroidal Na,K-ATPase activity. (J Histochem Cytochem 46: 975-976, 1998)

4-Nitrophenylphosphatase↗

PubMed2004

Antidepressant-like effect of tramadol and its enantiomers in reserpinized mice: comparative study with desipramine, fluvoxamine, venlafaxine and opiates.

Tramadol is a centrally acting analgesic that demonstrates opioid and monoaminergic properties. Several studies have suggested that tramadol could play a role in mood improvement. Moreover, it has previously been shown that tramadol is effective in the forced swimming test in mice and the learned helplessness model in rats, two behavioural models predictive of antidepressant activity. The aim of the present study was to test tramadol and its enantiomers in the reserpine test in mice, a classical observational test widely used in the screening of antidepressant drugs. This test is a non-behavioural method where only objective parameters such as rectal temperature and palprebral ptosis are considered. Moreover, we compared the effects of tramadol and its enantiomers with those of antidepressants (desipramine, fluvoxamine and venlafaxine) and opiates [morphine (-)-methadone and levorphanol]. Racemic tramadol, (-)-tramadol, desipramine and venlafaxine reversed the reserpine syndrome (rectal temperature and ptosis), whereas(+)-tramadol and fluvoxamine only antagonized the reserpine-induced ptosis, without any effect on temperature. Opiates did not reverse reserpine-induced hypothermia. (-)-Methadone showed slight effects regarding reserpine-induced ptosis, morphine and levorphanol had no effect. These results show that tramadol has an effect comparable to clinically effective antidepressants in a test predictive of antidepressant activity, without behavioural implications. Together with other clinical and experimental data, this suggests that tramadol has an inherent antidepressant-like (mood improving) activity, and that this effect could have clinical repercussions on the affective component of pain.

Analgesics, Opioid↗

PubMed1989

Light and electron microscopy of the exocrine pancreas in the chronically reserpinized rat.

The effects of reserpine injections were studied on the morphology of the pancreas in an experimental model for cystic fibrosis, the chronically reserpinized rat. A detailed examination of the tissue was carried out at the light and electron microscopic levels. The nonspecific effects of secondary malnutrition induced by the drug were assessed with a group of animals pair fed with the treated animals. In a companion paper, we show that pancreatic wt, lipase, and GP-2 contents also are affected by reserpine treatment. In this study, we report that no morphologic differences were observed between the exocrine pancreatic tissue of control and pair-fed animals. By contrast, reserpine induced an accumulation of zymogen granules in 60% of the treated animals and a concomitant decrease of the area occupied by the rough endoplasmic reticulum in the same cells. Finally, in all treated animals, at the light and electron microscopic levels, it was observed that some particular regions of the pancreatic tissue were strongly affected. In these regions, numerous autophagic bodies and lysosomes were observed. Cisternae of the Golgi complex were also more distended. Some acinar cells were in the process of lysis. Several vacuolar inclusions were present in some intralobular duct cells. Cellular material was seen in acinar and intralobular duct lumina. In these same regions, distended intralobular ducts and acinar lumina were observed. These last two features have never been reported in the reserpinized rat but are important manifestations of the pathology in cystic fibrosis patients where obstructions of ducts are believed to trigger focal destruction of the pancreatic tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

Monoaminergic control of episodic growth hormone secretion in the rat: effects of reserpine, alpha-methyl-p-tyrosine, p-chlorophenylalanine, and haloperidol.

The effects on GH secretion of reserpine, alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA), and haloperidol were studied in undisturbed, unanesthetized male rats with implanted intraaortic cannulae. The effects of the various drug treatments on motor activity and brain levels of catecholamines (CAs) and 5-hydroxytryptamine (5-HT) as well as the synthesis of the biogenic amines were also studied. Reserpine (10 mg/kg, ip) completely inhibited GH secretion for at least 15 h. Repeated injections of reserpine prolonged this inhibition. Episodic GH secretion reappeared 36 h after the last administration of reserpine, at which time the behavioral inhibition and blepharospasm induced by the drug was less pronounced than after 24 h, but brain levels of CAs and 5-HT were still markedly reduced. Administration of alpha-MT (150 mg/kg; 12, 4, and 2 h before experiments) inhibited episodic GH secretion and caused marked inhibition of motor activity and brain levels of CAs but not 5-HT. The inhibition of episodic GH secretion was more pronounced with haloperidol (0.5 mg/kg; 30 min before experiments) than with alpha-MT but was not as complete as that found 12 h after administration of reserpine. Administration of p-chlorophenylalanine (300 mg/kg; 72, 48, and 24 h before experiments) had no effect on episodic GH secretion, whereas brain levels of 5-HT and 5-HT synthesis were markedly reduced.

Animals↗

PubMed1985

[A TRH analog (DN-1417). Anti-reserpine action in electroconvulsive threshold and involvement of serotonergic (5-HT) mechanism in mice].

The antagonistic effect of a TRH (Thyrotropin-releasing hormone) analog, DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide citrate) against reserpine-induced reduction of electroconvulsive threshold (EC50) and the involvement of monoaminergic mechanism were studied in mice. Reserpine (2 mg/kg, i.p.) reduced the EC50 to 55-77% of the control in association with the depletion of brain monoamine. TRH and DN-1417 significantly reversed the EC50 reduced by reserpine. DN-1417 partially recovered 5-HT level and increased in the brain levels of 3-methoxy-4-hydroxyphenylglycol, homovanillic acid and 5-hydroxyindoleacetic acid in reserpinized mice. Monoaminergic receptor blockers attenuated, but muscarinic blockers accelerated the antagonistic effects of DN-1417 on the EC50. Neither alpha-methyl-p-tyrosine nor FLA-63 inhibited the effects of DN-1417, whereas p-chlorophenylalanine not only inhibited the antagonistic effect of DN-1417 on the EC50 but also prevented the stimulation effect on 5-HT turnover. Therefore, the antagonistic effect of DN-1417 against reserpine on the EC50 is most likely mediated by the stimulation of monoamine turnover, especially 5-HT in mice.

5-Hydroxytryptophan↗

PubMed1975

Sympathomimetic actions of reserpine administered during treatment with dopamine in the dog.

Reserpine injected intravenously during infusion with dopamine brought about sympathomimetic effects, but a second injection of reserpine after 120 minutes did not elicit such effects. This pressor effect was eliminated by phenoxybenzamine and this positive chronotrpic effect by propranolol. Reserpine induced similar but weak sympathomimetic effects after cocaine, while it induced no changes in blood pressure and heart rate after infusion with noradrenaline. Meanwhile, pressor response to dopamine was potentiated 24 hours after reserpine and was further potentiated after additional infusion with noradrenaline. The sympathomimetic actions induced by the concurrent administration of reserpine and dopamine may be attributable to a facilitation of those indirect mechanisms, prinicpally of endogenous catecholamine release.

Animals↗

PubMed1995

The role of L-threo DOPS in the control of Na-K ATPase activity of the marginal cells in the stria vascularis of reserpinized guinea pigs.

It is believed that the function of the stria vascularis in the cochlea is to produce endolymph. The mechanisms that maintain or control the function of the stria vascularis, however, remain unclear. In a previous study, we investigated the ultracytochemical effects of one-shot reserpine administration on the Na-K ATPase activity of the stria vascularis in guinea pigs. Na-K ATPase activity was shown to be completely inhibited 3-20 days after reserpinization, whereas in the present study at 20 days after reserpinization and following L-threo DOPS treatment, Na-K ATPase activity was detectable. As reserpine is an adrenergic neuron blocker, and L-threo DOPS is the precursor of noradrenaline, it seems that noradrenaline converted from L-threo DOPS was able to restore the Na-K ATPase activity in the reserpinized animals. These results suggest that catecholamines may play an essential role in the maintenance or control of the Na-K ATPase activity, and that the stria vascularis may be one of the target organs of catecholamines.

4-Nitrophenylphosphatase↗

PubMedDate not supplied

The reserpinized rat in the study of cystic fibrosis: x-ray microanalysis of submandibular gland and pancreas.

The chronically reserpinized rat has been suggested as an animal model for cystic fibrosis. X-ray microanalysis of thick and thin cryosections was carried out to assess elemental redistribution in the submandibular glands and the pancreas of reserpinized rats at the cellular and subcellular level. In the submandibular gland of reserpinized rats, calcium and magnesium concentrations were significantly elevated. Mucus globules, secretory granules, and endoplasmic reticulum were the primary sites of the localization of excess calcium and magnesium. A significant potassium loss from the gland had occurred, particularly from the serous cells. Electron microscopy of conventionally prepared tissue showed marked swelling of the endoplasmic reticulum, especially in mucous cells. The elemental changes in the pancreatic acinar cells of reserpinized rats were reminiscent of elemental redistribution connected with cell death: increased levels of sodium, chlorine, and calcium and decreased levels of magnesium and potassium. Ultrastructural changes included swelling of the endoplasmic reticulum and obstruction of the acinar lumen. It is concluded tha elemental redistribution in chronically reserpinized rats presents interesting parallels with cystic fibrosis.

Animals↗

PubMed1997

A simple, non-invasive method for the measurement of reserpine-induced tremor in rats.

A new, non-invasive method for measuring reserpine-induced tremor in rodents is described here. The test procedure is based on the piezo-electric principle and was evaluated using the tremorogenic compound reserpine and the stereotypies-inducing drug apomorphine. Whereas for reserpine an orderly and dose-related increase in activity was observed, no such effect was detected with apomorphine. In order to further evaluate the test procedure, studies on the antagonism of reserpine-induced tremor were also performed. Results from these studies indicated that the DA-agonist lisuride, but not the S2-antagonist ritanserin, were able to antagonize the reserpine-induced tremor in a dose-related manner.

Animals↗

PubMed1975

Abnormal secretory response to parasympathomimetic and sympathomimetic stimulations from the submaxillary gland of rats treated with reserpine.

Rats treated with 0.5 mg/kg of reserpine per day for 7 days were anesthetized and submaxillary saliva was collected and analyzed for Na+, K+, Ca++ and protein concentrations. Salivary secretion was elicited by i.p. injections of carbamylcholine (50-100 mug/kg), phenylephrine (5 mg/kg) and isoproterenol (10 mg/rat). Saliva was also collected from untreated controls. Submaxillary glands were excised from both groups of animals at the termination of the secretory response, homogenized and analyzed. Glands from other animals were removed in the resting state and similarly processed. Pretreatment with reserpine resulted in decreased volumes of salvia and in elevated salivary concentrations of Ca++ and protein. Saliva from the reserpine-treated animals secreted in response to carbamylcholine had higher concentrations of Na+ and K+ than control saliva, particularly at the low rates of flow. Saliva secreted after stimulation with the two sympathomimetic secretagogues had lower concentrations of these two ions. Resting glands from the treated animals showed significant elevations in protein and Ca++ content and a significant decrease in K+ content. At the end of the secretory response to the three secretagogues, glands from treated animals showed a significantly higher Na+ content and a significantly lower K+ content than control glands. It is concluded that pretreatment with reserpine alters the secretory response of the rat submaxillary gland to both parasympathomimetic and sympathomimetic stimulation. This alteration results from a toxic lesion caused by reserpine in the salivary cells, which involves changes in their permeability to ions and in their energy resources. These in turn, result in an abnormal stimulus-secretion coupling mechanism. The possibility that the toxic lesion is related to alterations in Ca++ homeostasis is discussed.

Animals↗

PubMed1992

D1 receptor stimulation inhibits dopamine cell activity after reserpine treatment but not after chronic SCH 23390: an effect blocked by N-methyl-D-aspartate antagonists.

Single unit recordings were conducted to examine the effects of systemic D1 agonist SKF 38393 on the firing rate of substantia nigra pars compacta dopamine (DA) neurons in rats pretreated subchronically with reserpine or chronically with a D1 antagonist. The effect of N-methyl-D-aspartate receptor antagonists on these processes was also investigated. An i.v. injection of SKF 38393 (10 mg/kg) significantly inhibited DA cell activity by approximately 70% in rats pretreated with reserpine (1 mg/kg, s.c.) for 6 days and studied under conditions of local anesthesia. SKF 38393 exerted no effect in reserpinized rats anesthetized with chloral hydrate. The SKF 38393-induced inhibition was reversed by the D1 antagonist SCH 23390, but not by the preferential D2 antagonist haloperidol. This effect of SKF 38393 was observed in 60% of the rats as early as 3 to 8 hr after the first reserpine injection, and the inhibition remained significant 5 to 15 days (averaging 64 and 58%) after termination of the 6-day reserpine treatment. The N-methyl-D-aspartate antagonists ketamine, at anesthetic doses (100 mg/kg, i.p.), and MK 801, at a nonanesthetic dose (0.15 mg/kg, i.v.), completely blocked the inhibitory effect of SKF 38393. In contrast, DA cells recorded in rats pretreated with SCH 23390 for 7 to 21 days, followed by a 4-day washout period, failed to respond to SKF 38393. Because nigrostriatal DA neurons do not appear to express D1 receptors, these results suggest that D1 receptors can exert an indirect inhibitory effect on the activity of nigral DA neurons, presumably through striatonigral neuronal pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1975

Influence of reserpine on all-night sleep pattern in nonlobotomized and lobotomized chronic schizophrenic patients.

This study was performed on two groups of schizophrenic patients. One group consisted on nine nonlobotomized patients and the other of nine lobotomized ones. The groups were matched for age, sex, duration of illness, clinical symptoms, type and dose of psychopharmacological treatment. The patients of both groups were administered 1 mg of reserpine half an hour before bedtime, for three successive days. Before reserpine administration the mean percentage time of the NREM stage 4 was significantly higher in the lobotomized group. There was no significant difference in the REM parameters. After three days of reserpine administration in the nonlobotomized group, there was no significant difference in the mean percentage of the NREM stage 4, whereas the mean REM percentage significantly increased and REM latency decreased. In the lobotomized group the same procedure, i.e., three days of reserpine administration, provoked a significant decrease in the mean percentage of the NREM stage 4 and no significant changes in the REM parameters. This difference in reserpine action on sleep in the lobotomized group is discussed.

Chronic Disease↗

PubMed1975

Reserpine induced changes in the estradiol uptake by the pituitary and the uterus in ovariectomized rats.

Reserpine treatment produced a marked decrease of the in vitro binding of estradiol to the nuclear fraction of the uterus. A similar observation was made when reserpine was given into the incubation medium of uterine tissue. In contrast to these findings both in vitro and in vivo reserpine administration resulted in an increase of the estradiol binding to the nuclear fraction of the anterior pituitary in ovariectomized rats. The binding capacity of cytosol fraction after reserpine administration did not show significant alterations. In addition to these observations it is worth to mention that reserpine treatment resulted in a significant decrease of the estradiol-induced increase of uterus weight in ovariectomized rats.

Animals↗

PubMed2006

Protective effect of centrally-injected glucagon-like peptide-1 on reserpine-induced gastric mucosal lesions in rat: possible mechanisms.

BACKGROUND/AIMS: Intracerebroventricular glucagon-like peptide- 1 (GLP-1) has been shown to prevent the gastric mucosal lesions induced by reserpine. In the present study, we aimed to investigate the contribution of 1- the cholinergic pathway, 2- the sympathetic pathway, 3- somatostatin and 4- endogenous nitric oxide to this gastroprotective effect. METHODS: Rats were equipped with intravenous and intracerebroventricular cannulas under ether anesthesia for drug delivery. Rats were pretreated with mecamylamine (5 mg/kg; i.p.) and atropine sulfate (1 mg/kg; i.p.), yohimbine (1 mg/kg; i.p.), cysteamine (280 mg/kg; s.c.), and NG-nitro-L-arginine methyl ester (3 mg/kg; i.v.) to investigate the role of the cholinergic pathway, sympathetic pathway, somatostatin and endogenous nitric oxide, respectively, in the gastroprotective effect of GLP-1. To produce gastric mucosal lesions, reserpine was administered intraperitoneally at a dose of 25 mg/kg in 10 ml/kg of 0.5% acetic acid solution. Four hours later, the animals were decapitated, and their stomachs were removed and scored for mucosal damage. RESULTS: Glucagon- like peptide-1 (100 ng/10 microl; i.c.v.) inhibited the reserpine-induced gastric mucosal damage by 90% (p<0.01). Neither the nicotinic receptor antagonist mecamylamine (5 mg/kg; i.p.) nor the muscarinic receptor antagonist atropine sulfate (1 mg/kg; i.p) affected the gastroprotective activity of GLP-1. On the other hand, pretreatment with yohimbine, an alpha2-adrenergic receptor antagonist (1 mg/kg; i.p.), cysteamine, a somatostatin depletor (280 mg/kg; s.c.), and NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor (3 mg/kg; i.v.), significantly abolished the protective effect of GLP-1 on reserpine-induced gastric mucosal lesions (p<0.001, p<0.01 and p<0.01, respectively). CONCLUSIONS: We conclude that the sympathetic pathway, somatostatin and nitric oxide, but not the cholinergic pathway, contribute to the gastroprotective effect of intra-cerebroventricular GLP-1 on reserpine-induced gastric mucosal lesions.

Adrenergic Uptake Inhibitors↗

PubMed1990

Long lasting increase in neuropeptide Y gene expression in rat adrenal gland with reserpine treatment: positive regulation of transsynaptic activation and membrane depolarization.

To elucidate how the neuropeptide Y (NPY) gene is regulated by physiological/pharmacological changes in neural functions, the expression and regulation of the NPY gene were studied by measuring changes in the abundances of NPY and NPY mRNA in the adrenal gland and brain regions of rats in vivo and in PC12 rat pheochromocytoma cells after reserpine treatment. Long term treatment with reserpine in vivo, which causes hypotension and increased splanchnic nerve activity, induced prolonged increases in the abundance of NPY mRNA and putative NPY pre-mRNA, with concomitant increases in NPY, in the adrenal gland in a tissue-dependent manner but caused no changes in the abundance of beta-actin mRNA. Transection of the splanchnic nerves almost completely (76%) prevented the reserpine-induced increases in the abundance of NPY mRNA and NPY pre-mRNA, but denervation alone did not affect their steady state levels. These results suggested that increased activity of the splanchnic nerves regulates NPY gene expression positively in the adrenal gland, probably at the level of transcription. In PC12 cells, reserpine decreased the abundance of NPY mRNA directly, but nicotinic receptor activation increased its abundance transiently and the persistent membrane depolarization increased its abundance markedly. Thus, NPY gene expression is positively regulated by membrane depolarization via increased transsynaptic activation with reserpine.

Actins↗

PubMed1979

Ability of aged rats to alter beta adrenergic receptors of brain in response to repeated administration of reserpine and desmethylimipramine.

Repeated administration of reserpine to 3-month-old rats produced dose-related increases in [3H]dihydroalprenolol (DHA) binding in pineal gland, cerebral cortex and cerebellum. Reserpine increased DHA binding by increasing the density of beta adrenergic receptors. Brain tissue from 24-month-old rats, however, had an impaired ability to increase receptor density in response to reserpine treatment, even in the pineal gland where the concentration of reserpine was nearly 7 times that found in the glands of young rats given the same dose on the basis of body weight. Repeated administration of desmethylimipramine decreased DHA binding in pineal glands by about 50% and in cerebral cortices by about 25%, but did not alter DHA binding in the cerebellum. The magnitude of these changes was similar in the 3- and 24-month-old rats, although the concentration of desmethylimipramine in the pineal glands and cerebral cortices of the aged rats was significantly higher than that of the young animals. The results indicate that the reserpine-induced decrease in noradrenergic input causes a compensatory increase in beta adrenergic receptor density in rat brain. They suggest further that although aged rats can decrease receptor density in response to increased adrenergic input, they have an impaired ability to increase beta adrenergic receptor density in response to decreased adrenergic input. This finding may explain the decreased density of beta adrenergic receptor found in aged rat brain.

Aging↗

PubMed1986

[Overcoming of ACNU resistance in a subline of rat glioma in vitro and in vivo by reserpine].

Reserpine was shown to enhance the cytotoxicity of ACNU in both C6 and C6/ACNU rat glioma cells in vitro and also to enhance the chemotherapeutic effect of ACNU in C6/ACNU-bearing rats (C6/ACNU meningeal gliomatosis rats), in which ACNU resistance could be partially overcome by reserpine. When reserpine was added to the culture at a concentration of 10 microM, the IC50 of ACNU for C6/ACNU cells decreased to the level of that for C6 cells. Intracellular uptake of ACNU in C6/ACNU cells increased and the efflux from the cells decreased when 20 microM reserpine was added to the culture. In in vivo experiments, combined ACNU (1 mg/kg) and reserpine (250 micrograms/kg) therapy by intrathecal injection of these drugs improved % ILS (increased life span) with statistical significance compared with that after treatment with ACNU alone. The probable explanation of the enhanced cytotoxic-effect of ACNU in ACNU-resistant glioma cells presented in in vitro and in vivo is increased intracellular ACNU concentration resulting from inhibition of the efflux of ACNU from the resistant cells.

Animals↗

PubMed1987

Effect of reserpine on the performance of broiler chicks.

The effect was studied of tranquilizer reserpine on the performance of Hubbard chicks. The results can be summed up as follows: The supplementation with reserpine at levels of 0.25 and 0.5 ppm decreased the final body weight, and the growth depression was more pronounced at the higher doses. Supplementation by 0.25 ppm reserpine improved the feed efficiency as compared with the control group, whereas this efficiency deteriorated on supplementation with 0.5 ppm. The mortality rates were 13.5% for the control group and 0.0 and 2.7% for the groups with 0.25 and 0.5 ppm of reserpine, respectively. Reserpine supplementation had no significant effect on the percentage of the dressing carcass, edible giblets, feathers, head and feet.

Analysis of Variance↗