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At least 1,153 records · Page 64Linked to original sources
PubMed1986

The effect of 6-hydroxydopamine, reserpine and cold stress on the neuropeptide Y content of the rat central nervous system.

Neuropeptide Y has previously been detected in neurons throughout the rat brain and spinal cord. On histochemical grounds, the neuropeptide Y-containing cell bodies have been subdivided into two groups: those in the brain stem in which colocalization with noradrenaline and adrenaline has been demonstrated and those in other brain regions where no catecholamine coexistence is found. In this paper the regional distribution of neuropeptide Y has been investigated in the rat brain by a specific neuropeptide Y radioimmunoassay, before and after the destruction of catecholaminergic nerve terminals by the administration of intraventricular 6-hydroxydopamine. Despite massive reductions in brain catecholamines, the neuropeptide Y level was unchanged in the cerebral cortex, striatum, spinal cord and hippocampus. A minor reduction in neuropeptide Y was found in the hypothalamus. Reserpine treatment, which is known to deplete brain nerve terminal stores of catecholamines, likewise did not result in any loss of neuropeptide Y. Cold stress which increases noradrenergic turnover in the rat brain stem had no effect on neuropeptide Y levels. These results suggest that the bulk of neuropeptide Y in the rat brain and spinal cord may not be stored in catecholaminergic nerve terminals.

Animals↗
PubMed1988

Clenbuterol stimulated increase of plasma free fatty acids in reserpinized pigs.

1. Previous studies indicate the beta-adrenergic agonist, clenbuterol, does not stimulate porcine adipose tissue lipolysis or cAMP concentration in vitro but increases plasma free fatty acid concentrations when infused, implying an indirect mechanism in vivo. 2. One indirect mechanism is the release of endogenous catecholamines to increase adipose tissue lipolysis and raise plasma free fatty acids. 3. In pigs treated with reserpine to deplete endogenous catecholamines, clenbuterol infusion increased plasma free fatty acids concentration suggesting that this increase in vivo did not result from release of endogenous catecholamines.

Animals↗
PubMed1988

Actions of dopamine and related amines on reserpinized and chronically denervated vasa deferentia of the rat.

1. Reserpine, chronic guanethidine denervation and alpha-adrenoceptor antagonists were used to distinguish between presynaptic and postsynaptic actions of exogenous dopamine (DA), octopamine (OA), tyramine (TA) and noradrenaline (NA) on the rat vas deferens. 2. TA has only a presynaptic action while DA and OA have mixed presynaptic actions (releasing endogenous NA) and postsynaptic actions. 3. The postsynaptic actions of DA and OA are likely to be mediated by alpha-adrenoceptors rather than by specific receptors.

Amines↗
PubMed1990

Intravenous regional sympatholysis: a double-blind comparison of guanethidine, reserpine, and normal saline.

This double-blind, randomized study was designed to compare the effectiveness of intravenous regional sympatholysis using guanethidine, reserpine and normal saline. Twenty-one patients with reflex sympathetic dystrophy of an upper or lower extremity were enrolled and received intravenous regional blockade (IVRB) with one of the three medications. There was significant pain relief in all three groups at 30 min. There were no significant differences among the three groups in the degree of pain relief, the number of patients obtaining pain relief in the 30 min after the block, or the number of patients reporting more than 50% pain relief for more than 24 hr. The saline group's high rate of pain relief could be partially due to a mechanism of tourniquet-induced analgesia.

Adult↗
PubMed2004

Effect of adrenomedullin on c-Met receptor expression after reserpine-induced gastric damage in the rat.

Here, we show an increase in c-Met receptor expression during reserpine-induced gastric damage in the rat, as assessed by immunohistochemistry. Pretreatment of animals with adrenomedullin prevented this increase in c-Met expression. c-Met immunoreactivity was localized in gastric glands. c-Met immunoreactivity was associated with increased phosphorylation of c-Met receptor and extracellular signal-regulated kinase (ERK(1/2)). Our results suggest that both adrenomedullin and c-Met act as parallel defence mechanisms during pharmacologically induced gastric mucosa injury.

Adrenomedullin↗
PubMed1998

Effects of centrally of peripherally injected adrenomedullin on reserpine-induced gastric lesions.

Adrenomedullin intracerebroventricularly administered (0.1 to 20 ng/rat i.c.v.), showed significant gastroprotective activity in a dose-dependent manner. When the peptide was intravenously administered (1 to 1000 ng/kg i.v.) it did not show significant gastroprotective activity in the same test. The gastroprotective effect of the peptide (10 ng/rat) was abolished by bilateral adrenalectomy, by pretreatment with the beta-adrenoceptor antagonist, propranolol (1 mg/kg i.p.), or by a calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP-(8-37) fragment (1 or 10 ng/rat i.c.v.). This study showed that adrenomedullin is protective against reserpine-induced gastric lesions, that the action involves sympathetic nerve activity, and moreover interferes with CGRP receptors.

Adrenalectomy↗
PubMed1988

The kallikrein kinin system in pulmonary lavage fluid of reserpinized rats.

Kallikrein content in lavage of the respiratory tract was determined by a specific RIA. The results show an immunological identity of the lung kallikrein with the standard rat urinary kallikrein. The levels of immunoreactive lung fluid kallikrein were significantly lower in rats injected with reserpine.

Animals↗
PubMed1975

The possible mode of action of prostaglandins: VIII - cortisone, reserpine and the reversal of the antifertility efficacy of prostaglandin E1 in rats.

A single injection of prostaglandin F1 (PGE1) of 5 mg/kg body weight on Lay 13 of pregnancy caused a consistent luteolysis and resorption of fetuses in rats by Day 20. A concomitant regimen of cortisone, a consistent blocker of nonspecific stresses or reserpine, an adrenergic nerve blocking agent as well as a specific inhibitor of GRF and PIF, concurrently with PGE1 consistently effective in preventing the deleterious efficacy of PGE1 and maintained the growth of the fetuses, placentae, ovaries and corpora lutea as healthy as recorded in the controls. On the basis of experimental documentation it is believed that the PGE1-caused fetal demise is possibly due to a break up of an appropriate hormonal synchronization rather than an over stimulation of uterine smooth musculature.

Animals↗
PubMedDate not supplied

Effect of amantadine on chlorpromazine and reserpine-induced behavioral depression in the mouse.

The effect of pretreatment with amantadine (AMN) on chlorpromazine (CPZ) and reserpine (RES)-produced behavioral depression was studied in the male mouse. The effect of this treatment on hepatic alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH), which catalyze the metabolism of biogenic amine aldehydes, was also investigated. Administration of AMN, 100 mg/kg, initially decreased spontaneous locomotor activity from saline control. Pretreatment with identical dose of AMN 15 min before small dose of CPZ or RES, 0.2 mg/kg, further suppressed motility compared to animals receiving the individual AMN, CPZ or RES treatment. Using a second dose regimen of these compounds, given 5 hr post the initial injection, altered L-ALDH as a function of its subcellular localization. This was demonstrated by AMN-produced induction of mitochondrial, but not cytoplasmic L-ALDH. Likewise, a moderate but not statistically significant increase in endogenous mitochondrial L-ALDH was determined subsequent to the CPZ treatment. Treatment with AMN prior to CPZ reduced the enhancement of L-ALDH to control levels. The RES dose used was devoid of action on remainder of hepatic enzymes measured. The results indicate that AMN possesses central depressant property which was potentiated by CPZ and RES. The enzymatic data suggest antagonism between AMN and CPZ on induction of mitochondrial L-ALDH.

Alcohol Dehydrogenase↗
PubMed2002

Evaluation of the face validity of reserpine administration as an animal model of depression--Parkinson's disease association.

The aim of the present study was to develop an animal model for the study of depressive symptoms associated with Parkinson's disease (PD). Mice treated intraperitoneally with reserpine (RES), 2.0 and 1.0 mg/kg, or its vehicle (VEHIC) were submitted to the sucrose solution (2%) consumption test (a model employed to mimic the depressive symptoms found in PD) and to the spontaneous locomotor activity test (a model employed to mimic the motor impairment found in PD). All animals were submitted to both tests. Twenty-four hours after treatment, only RES 2.0-treated animals showed a significantly decreased preference for the sucrose solution (mean +/- S.E.M. RES 2.0 = 54.4 +/- 4.1%, RES 1.0 = 68.5 +/- 2.5%, VEHIC = 62.3 +/- 4.1%). There was no significant difference among groups in water, sucrose or total fluid consumption. Locomotor activity was significantly decreased by both RES doses (number of beam interruptions: RES 2.0 = 59.9 +/- 11.4, RES 1.0 = 82.2 +/- 9.7, VEHIC = 116.8 +/- 8.2). Thus, RES 2.0 administration to mice induced depressive (anhedonia) and motor (decreased locomotor activity) symptoms of depression-PD association. This suggests that the RES model shows an important aspect of face validity for the depressive state associated with PD, i.e., phenomenological similarities between the model and the situation being modeled.

Animals↗
PubMed2003

Vitamin E attenuates reserpine-induced oral dyskinesia and striatal oxidized glutathione/reduced glutathione ratio (GSSG/GSH) enhancement in rats.

The effects of a previous and concomitant treatment with vitamin E (VE) were studied on an animal model of tardive dyskinesia, i.e., the frequency of spontaneous tongue protrusions in rats treated with reserpine (RE). VE (5, 10, 20 or 40 mg/kg administered intraperitoneally, daily, for 19 days) attenuated the increase in tongue protrusion frequency induced by RE (1 mg/kg administered subcutaneously, on Days 16 and 18, 1 h after VE), which was quantified on Day 19. In a second experiment, a similar treatment with 20 mg/kg VE attenuated RE-induced increase in the striatal ratio of oxidized/reduced glutathione (GSSG/GSH), an index of the oxidative stress process. These results support the free radical hypothesis of tardive dyskinesia.

Adrenergic Uptake Inhibitors↗
PubMed1997

Differential effects of intrastriatal and intranigral injections of glutamate antagonists on motor behaviour in the reserpine-treated rat.

A variety of N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonists, and the antiepileptic drug lamotrigine, were examined for their ability to restore locomotion and other behaviours when injected stereotaxically via indwelling cannulae into the striatum or substantia nigra pars reticulata of rats rendered akinetic with reserpine (5 mg/kg i.p. 24 h beforehand). Only the competitive N-methyl-D-aspartate antagonists 3-((+)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate and R-DL-(E)-2-amino-4-methyl-5-phosphono-3-pentanoate stimulated locomotion from the striatum, whereas 2-amino-phosphonopentanoic acid, the N-methyl-D-aspartate channel blockers dizocilpine maleate and phencyclidine, and the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid antagonist 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(f)-quinoxaline-dione, were additionally effective in the substantia nigra pars reticulata. The N-methyl-D-aspartate glycine site antagonist (RS)-3-amino-1-hydroxypyrrolidin-2-one and the glutamate release inhibitor lamotrigine failed to restore locomotion at these sites, and the N-methyl-D-aspartate polyamine site antagonist eliprodil was ineffective in the substantia nigra pars reticulata, although all compounds tested (except lamotrigine) induced orofacial, head and/or limb movements to some degree. Except for 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(f)-quinoxaline-dione, locomotion was accompanied dose-dependently by increasingly pronounced ataxia and postural abnormalities. These results show that the monoamine-depleted substantia nigra pars reticulata has a broader spectrum of responsitivity to the antiparkinsonian actions of N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid antagonists than does the striatum, and that the harmful as well as the beneficial effects of these compounds on locomotion arise from these two structures.

Animals↗
PubMed1998

Mitogenic short-term effects on hepatocytes and adrenocortical cells: phenobarbital and reserpine compared to carcinogenic and non-carcinogenic fluorene derivatives.

The adrenal cortex has a low physiologic cell renewal and shows only a moderate cell replication even after contralateral adrenalectomy. Although rather unsusceptible to the malignancy-inducing action of carcinogens, a single oral dose of various tumorigenic xenobiotics induced an additive mitotic response of adrenocortical cells studied after 48 h. Presently we report on three different response patterns in rats. First, a selective mitostimulation of the zona glomerulosa occured after reserpine associated with a loss of body weight, thymus and liver weight. These are unspecific stress effects and occur also after exogenous ACTH. Second, hepatomitogenic and liver-enlarging congeners, e.g. fluorene (FEN), fluorenone (FON) and 4-benzoyl-FON, but also the genotoxic 2-acetylaminofluorene (2-AAF) and 2,4,7-trinitro-FON induced a selective mitotic response of the zona fasciculata (ZF). After the lowest effective dose of FEN or FON the afore-mentioned effects occured simultaneously, but were absent in the high dose group (only studied with fluorene). The 2-benzyl and 2-benzoyl-substituted derivatives were ineffective at all. Third, a bizonal response was found only after phenobarbital (PB) or the lowest effective FEN dose. The preventive action of a low PB dose on the 2-AAF-induced ZF response indicates a modified metabolism. We conclude that the rapid mitotic ZF response is an endogenously mediated net effect of interactions between metabolic and various adaptive mechanisms. The latter are reported to be activated in a stressor-dependent manner and converge in the adrenals. In this way the early mitotic ZF response could reflect indirectly 'specific' proliferation-prone properties of xenobiotics.

Adrenal Cortex↗
PubMed1989

Reserpine binding to chromaffin granules suggests the existence of two conformations of the monoamine transporter.

The binding of [3H]reserpine ([3H]RES) to purified bovine chromaffin granule membranes has been studied at low membrane concentration. Saturation isotherms indicated a dissociation equilibrium constant KD of 30 pM and a density of binding sites of 8 pmol/mg of protein at 30 degrees C. The association rate constant was 4.0 X 10(5) M-1 s-1, and the calculated dissociation rate constant was 1.2 X 10(-5) s-1, corresponding to a half-lifetime of about 16 h. Although this dissociation was too low to be measured directly, [3H]RES binding was indeed reversible since it was lost after addition of the detergent Triton X-100. Dihydrotetrabenazine (TBZOH) inhibited [3H]RES binding in a time-dependent manner, EC50 varying from 37 nM after a 1-h incubation to 600 nM after 16 h. On the contrary, [3H]RES binding inhibition by the substrate noradrenaline was time independent. It is proposed that the transporter exists in two different conformations which bind exclusively either tetrabenazine (TBZ) or RES and which are in equilibrium. The effects of detergents were consistent with this two-conformation model. The transporter solubilized by cholate bound [3H]TBZOH, but not [3H]RES. On the other hand, addition of cholate to membrane-bound [3H]RES solubilized the membrane without releasing the ligand from its binding site. It is proposed that the TBZ-binding conformation is obtained by solubilization with cholate and that RES stabilizes the RES-binding conformation, allowing its solubilization by this detergent.

Amines↗
PubMed2005

Synthesis of deserpidine from reserpine.

The Rauwolfia alkaloids reserpine (1) and deserpidine (2), two alkaloids from Rauwolfia species, have been widely used for their antihypertensive action. Deserpidine (2) is a compound with limited availability from natural sources, and its synthesis from 1 in six steps (41% overall yield) is reported here.

Molecular Structure↗
PubMed1980

alpha 2-Adrenergic receptors appear in rat salivary glands after reserpine treatment.

The regulation of central and peripheral adrenergic receptors by various chemical, physiological, pharmacological and pathological stimuli has been the subject of intense study. For example, drug treatments can produce relatively small changes in the density of existing receptor binding sites in a variety of tissues. The alpha-adrenergic receptors in rat salivary gland tissue have been studied using radioligand receptor binding techniques. We have recently identified and characterised alpha 1-adrenergic receptors in the rat submandibular gland, but surprisingly, alpha 2-adrenergic receptor binding was not detectable. We now report that a single treatment of reserpine results in the appearance of alpha 2-adrenergic binding sites within 12 h. Continued treatment with the drug produces further increases in the number of alpha 2-adrenergic receptors, such that after 7 days the levels of alpha 1- and alpha 2-adrenergic receptors are similar. This is the first example of a drug treatment resulting in the appearance of a receptor type which was not previously detectable.

Animals↗
PubMed2002

Effects of cocaine and reserpine administration on RNA editing of rat 5-HT2C receptor estimated by primer extension combined with denaturing high-performance liquid chromatography.

Serotonin 2C receptor (5-HT(2C)R) transcripts undergo RNA editing, generating pharmacologically different isoforms. To test whether the RNA editing of 5-HT(2C)R is regulated by serotonergic activity, effects of cocaine or reserpine administration in the rat cerebral cortex were examined. Although these drugs have been known to alter serotonin metabolism, no alterations in the RNA editing were found by the sequencing analysis. Towards high throughput analysis, we developed a non-RI method that allows accurate and rapid estimation of RNA editing by combining the primer extension with denaturing high-performance liquid chromatography (DHPLC). By using this, RNA editing efficiencies of 5-HT(2C)R in the midbrain and hippocampus as well as the cerebral cortex were examined, and no alterations were found among these regions. Our method using DHPLC is applicable to examine association of RNA editing with various diseases.

Amino Acid Sequence↗