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At least 883 records · Page 49Linked to original sources
PubMed1987

Time course study on the effect of reserpine on hypothalamic immunoreactive CRF levels in rats.

A time course study on the changes of rat hypothalamic corticotropin-releasing factor (CRF) levels and ACTH levels in plasma, pituitary and hypothalamus after an acute treatment with reserpine was examined using a rat CRF RIA. The massive and prolonged depletion of hypothalamic norepinephrine and dopamine levels provoked by a single injection of reserpine (2 and 8 mg/kg, i.p.) caused a transient decrease of hypothalamic CRF levels and ACTH levels in the anterior pituitary glands, and an increase in plasma ACTH levels. There was a strong correlation between the depletion of hypothalamic CRF and norepinephrine levels. These results suggest that: acute depletion of hypothalamic norepinephrine levels cause the initial release of CRF that stimulates pituitary ACTH secretion, and the depletion of CRF and ACTH stores at the early stage; and noradrenergic pathways may be involved in the inhibitory mechanism of CRF release.

Adrenocorticotropic Hormone↗
PubMed1987

Studies of the role of mast cells in contact sensitivity responses. Passive transfer of the reaction into mast cell-deficient mice locally reconstituted with cultured mast cells: effect of reserpine on transfer of the reaction with DNP-specific cloned T cells.

The role of mast cells in the elicitation of contact sensitivity (CS) responses was evaluated by transferring different aliquots of the same preparations of immune lymph node cells (I-LNC) into naive, genetically mast cell-deficient (WBB6F1-W/Wv or WCB6F1-S1/S1d) mice and the corresponding congenic normal (+/+) mice. We found that the 24-hr CS responses elicited in the recipient mast cell-deficient mice were statistically indistinguishable from those in the congenic +/+ mice according to four different criteria: micrometer measurements of ear swelling, ratios of the weight or [125I]iododeoxyuridine-labeled leukocyte infiltration-associated cpm in challenged and contralateral control ears, and amount of 125I-fibrin deposition. We also transferred I-LNC into WBB6F1-W/Wv mice which, 5 months earlier, had undergone local repair of their mast cell deficiency by the intradermal injection (into the left ear only) of growth factor-dependent cultured mast cells derived from congenic +/+ mice. When 24-hr CS responses were elicited in both ears of these mice, the reactions in the mast cell-reconstituted left ears were similar to those in the mast cell-deficient right ears. We also found that treatment of antigen-specific cloned T cells with reserpine in vitro markedly impaired their ability to transfer reactivity for CS, providing further evidence that reserpine can interfere with the expression of T-cell-mediated responses through effects independent of its action on mast cells.

Animals↗
PubMed1976

Effects of reserpine, guanethidine and methyldopa on cardiac output and its distribution.

In anaesthetized rats with a renal model of hypertension, effects of reserpine, guanethidine and methyldopa on cardiac output (the dye-dilution method) and its distribution among the heart, the lung, the kidney, the large and small intestine, the stomach, the liver, the spleen, skeletal muscle and skin (the rubidium method) were studied. Several hours administration of all three drugs under study, a definite decrease in cardiac output was observed. Cardiac output then escaped from the influence of the drugs despite a reduction in heart rate. Fall of arterial pressure 24 hr after administration of the drugs was only due to the decrease in total peripheral resistance. Effects of the drugs on distribution of cardiac output were studied at the time when cardiac output was not changed to any significant extent. Under this condition the features common to all the drugs were an increase of the cardiac output fractions to the gastro-intestinal tract and a decrease to the heart and the spleen. This fact indicates that decrease in resistance of gastro-intestinal vascular region plays a basic role in the hypotensive effect of reserpine, guanethidine and methyldopa.

Animals↗
PubMed1978

Reserpine-induced supersensitivity to the inotropic and phosphorylase activating effects of glucagon in the perfused rat heart.

Glucagon (0.125--2.0 microgram) produced a dose-dependent increase in cyclic AMP, % phosphorylase a and force of contraction in the isolated perfused rat heart. Pretreatment of animals with reserpine (2.5 mg/kg, 24 h) resulted in an enhancement of the inotropic and phosphorylase activating effects of glucagon but the effect on cyclic AMP was not altered. It is suggested that reserpine-induced supersensitivity in the rat heart occurs at a point beyond the cyclic AMP step.

Animals↗
PubMed1978

Chronic effects of 6-hydroxydopamine and reserpine on myocardial adenylate cyclase.

The effects of chronic administration of 6-hydroxydopamine or reserpine on catecholamine-sensitive adenylate cyclase from rat hearts were studied. Not only basal adenylate cyclase activity, but stimulation of the enzyme by norepinephrine, isoproterenol, NaF, guanylyl-imidodiphosphate, or combination of isoproterenol and guanylyl-imidodiphosphate, was significantly increased in the treated than in the control hearts. It is inferred that supersensitivity of myocardial adenylate cyclase following chronic treatment with reserpine or 6-hydroxydopamine may result from an increase in the catalytic activity of the enzyme.

Adenylyl Cyclases↗
PubMed1978

3H-Catecholamine binding to alpha-receptors in rat brain: enhancement by reserpine.

(+/-)-3H-Epinephrine and (-)-3H-norepinephrine bind to rat cortex membranes in a saturable manner with dissociation constants of 16.7 and 27 nM respectively. The maximum number of 3H-catecholamine binding sites, 10--12 pmoles/g tissue, and the pharmacological characteristics of (+/-)-3H-epinephrine binding, indicate that the catecholamines label the same alpha-noradrenergic receptor in the rat as does 3H-clonidine. At 25 degrees, (+/-)-3H-epinephrine binding associates rapidly to equilibrium, and dissociates in a biphasic manner. The affinities of alpha-agonists at the 3H-catecholamine binding site are 2--4 fold weaker in the rat than in the calf cortex under the same experimental conditions. Ergot alkaloids and phenoxybenzamine have similar affinities in the two tissues, whereas phentolamine and WB-4101 are 8--10 times weaker in the rat. Reserpine (0.25 mg/kg s.c. per day for 3 weeks) causes 25 and 46% increases in the numbers of (+/-)-3H-epinephrine and 3H-WB-4101 alpha-receptor binding sites respectively, and a 51% increase in the number of 3H-dihydroalprenolol beta-receptor sites, in rat forebrain. Reserpine pretreatment does not alter the affinities of either alpha- or beta-receptor 3H-ligands.

Animals↗
PubMed1982

Reserpine-induced supersensitivity and the proliferation of cardiac beta-adrenoceptors.

Chronic reserpine pretreatment resulted in an increase in the basal developed force generated by papillary muscles isolated from the right ventricle of the rabbit. In addition, supersensitivity to the inotropic effects of isoproterenol and a concomitant increase in beta-adrenoceptor number were demonstrated. These results indicate that reserpine-induced supersensitivity is not only associated with alterations at sites beyond the level of receptor activation but also at the level of specific postjuctional membrane receptors.

Adrenergic beta-Agonists↗
PubMed1983

The metabolic role of endogenous catecholamines in acute myocardial infarction: effects of reserpinization and of infused noradrenaline.

A significant decrease of the noradrenaline content of the ischemic as well as non-ischemic parts of the myocardium was found in rats after ligation of the left coronary artery. The eventual role of released noradrenaline in the anaerobic metabolism of the heart was investigated. A highly significant decrease of ATP and glycogen was obtained in the ischemic myocardium 10 min after coronary ligation whereas glucose-6-phosphate (g-6-p) was significantly increased. Catecholamine depletion by reserpine pretreatment did not reduce the loss of ATP, although the hearts had broken down rather higher amounts of glycogen. Glycolytic energy production was obviously inhibited, as the accumulation of g-6-p was significantly greater than in non-reserpinized animals. However when a high breakdown of glycogen was induced by noradrenaline infusion into coronary ligated animals, the g-6-p levels were no higher than those in untreated coronary-ligated rats. The results suggest that the ischemic breakdown of glycogen is independent of endogenous noradrenaline. The metabolic conversion of g-6-p, however, may need sufficient catecholaminergic stimulation to become fully activated.

Adenosine Triphosphate↗
PubMed1984

Electroshock-induced increase in [3H]prazosin binding to cortical membranes in reserpinized rats.

Chronic, spaced electroconvulsive shock (ECS, 6 treatments at 72 h intervals) produced a moderate (16%) increase in the density of [3H]prazosin binding sites to rat cerebral cortical membranes. The increase was of borderline significance (0.1 greater than P greater than 0.05) and KD was not affected. The effect was similar but much more pronounced (increase in Bmax by 38%, P less than 0.01) in rats receiving reserpine pretreatment (4 mg/kg i.p.) 24 h before each ECS. Reserpine produced a transient increase in [3H]prazosin binding 24 h but not 48 h after the last dose, at the time when the ECT effect was measured.

Animals↗
PubMed1986

Effects of pargyline, reserpine and neurotoxin lesions on [3H]tryptamine binding sites in rat brain.

[3H]Tryptamine binding sites were measured in 4 areas of rat brain following treatment with either pargyline or reserpine for 12 days, or 5 days and 30 days following intraventricular injections of 6-hydroxydopamine or 5,7-dihydroxytryptamine. Pargyline treatment decreased [3H]tryptamine binding in cerebral cortex, hippocampus, striatum and hypothalamus. Reserpine treatment increased binding in the cerebral cortex and hippocampus, but not in the striatum or hypothalamus. Neither 6-hydroxydopamine nor 5,7-dihydroxytryptamine altered [3H]tryptamine binding in any of the 4 brain areas. These results indicate that [3H]tryptamine binding sites in brain may be modified by drugs that can potentially affect tryptamine metabolism, and that the sites are not located on catecholamine or serotonin axons.

Animals↗
PubMed1987

Similarity of clozapine and SCH 23390 in reserpinized rats suggests a common mechanism of action.

Clozapine at doses up to 100 mg/kg p.o. did not antagonize apomorphine-induced stereotypy in vehicle pre-treated rats. However, if the animals were injected with reserpine (30 mg/kg i.p.) 24 h prior to the test, then clozapine (3-100 mg/kg p.o.) produced a dose-related blockade of apomorphine-induced stereotypy. The blockade of apomorphine-induced stereotypy in reserpinized rats by clozapine was attenuated by the D-2 selective agonist LY 171555 but not the D-1 selective agonist SKF 38393. This profile of agonist reversal of antagonist blockade of apomorphine-induced stereotypy seen with clozapine was identical to that seen with the selective D-1 antagonist SCH 23390. Presumably, the D-2 agonist was active because D-1 receptor systems were inhibited (either at the receptor or at some other post-synaptic site) by clozapine or SCH 23390; this allowed a partial restoration of apomorphine-induced stereotypy via the D-2 system. Therefore, these data indicate that clozapine and SCH 23390 share a common mechanism of action via D-1 receptor systems.

Animals↗
PubMed1988

Electroconvulsive shock and reserpine increase alpha 1-adrenoceptor binding sites but not norepinephrine-stimulated phosphoinositide hydrolysis in rat brain.

Repeated treatment of rats with either electroconvulsive shock or reserpine increased the density of alpha 1-adrenoceptor binding sites labeled by [3H]prazosin in rat frontal cerebral cortex. In contrast, norepinephrine-stimulated phosphoinositide hydrolysis, which is mediated by alpha 1-adrenoceptors, was not significantly affected by either treatment. These data suggest that electroconvulsive shock and reserpine might increase only or predominantly a subtype of alpha 1-adrenoceptor that is not coupled to phosphoinositide hydrolysis.

Animals↗
PubMed1991

Postsynaptic dopamine/adenosine interaction: I. Adenosine analogues inhibit dopamine D2-mediated behaviour in short-term reserpinized mice.

Mice pretreated with reserpine 5 mg/kg (4 h prior to the start of motor activity recording) showed locomotor activation after the administration of the D-2 agonist bromocriptine (5 mg/kg). This bromocriptine-induced locomotor activity was dose dependently inhibited by the co-administration of a D-2 antagonist (sulpiride) and dose dependently potentiated by a D-1 agonist (CY 208-243). The potentiating effect of the D-1 agonist could be inhibited by either a D-1 or a D-2 antagonist (SCH 23390 1 mg/kg or sulpiride 100 mg/kg, respectively). The bromocriptine-induced locomotor activity was not altered by either blockade of D-1 dopaminergic receptors (SCH 23390 1 mg/kg) or by co-administration of a greater dose of reserpine (10 mg/kg) plus the dopamine synthesis inhibitor, alpha-methyl-p-tyrosine (200 mg/kg). The adenosine agonists, L-PIA (a preferentially A-1 adenosine agonist) and NECA (an A-1 and A-2 adenosine agonist with above 10-fold greater affinity for A-2 than L-PIA) inhibited in a dose-dependent manner the effect of bromocriptine, NECA being above ten times more potent than L-PIA. The findings show that bromocriptine stimulates postsynaptic D-2 receptors in dopamine-depleted mice and that this effect can be inhibited by adenosine stimulation. The existence of a postsynaptic D-2/A-2 interaction is suggested, the stimulation of A-2 receptors causing an inhibition of responses elicited by postsynaptic D-2 stimulation.

Adenosine↗
PubMed1992

Repeated reserpine administration reduces in vivo [18F]GBR 13119 binding to the dopamine uptake site.

The effects of repeated reserpine on the in vivo regional brain distribution of [18F]GBR 13119 (1-[(4-[18F]fluorophenyl)(phenyl)methoxy)ethyl]-4-(3-phenylpropyl) piperazine), a dopamine uptake inhibitor, have been examined. Repeated parenteral administration of reserpine (2 mg/kg i.p., once daily for three days) causes a decrease of the in vivo specific binding of [18F]GBR 13119 in mouse striatum, consistent with a down-regulation of available uptake sites in response to dopamine depletion. These results indicate that modification of endogenous dopamine concentrations, either due to pathological disturbance or pharmacological interventions, may affect in vivo studies of the dopamine uptake system using radioligands of the 1,4-dialk(en)ylpiperazine class, and complicate the interpretation of in vivo human studies of these radioligands using positron emission tomography.

Animals↗
PubMed1993

Facilitation of dopamine D1 receptor- but not dopamine D1/D2 receptor-dependent locomotion by glutamate antagonists in the reserpine-treated mouse.

The effects of a selection of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonists on dopamine D1 and D2 receptor-dependent locomotor activity were studied in 24 h reserpine-treated mice. At fixed doses, determined from a previous study to be optimal for augmenting D1-dependent locomotion, 3-[(+)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP; 1 mg/kg), R-(E)-2-amino-4-methyl-5-phosphono-3-pentanoate (CGP 40116; 1 mg/kg), (RS)-3-amino-1-hydroxypyrrolidin-2-one (HA 966; 2 mg/kg), (+)-5-methyl-10,11-dihydro-5H-dibenzo-(a,d)-cyclohepten-5,10-imine (MK 801; 0.4 mg/kg) and 2,3-hydroxy-6-nitro-7-sulphamoyl-benzo(f)-quinoxaline-dione (NBQX; 0.2 mg/kg) all failed to reverse the akinesia of reserpine treatment by themselves. As expected, however, all five glutamate receptor antagonists potentiated locomotion induced by 30 mg/kg 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine hydrochloride (SKF 38393; D1 receptor agonist). Only CPP and MK 801 potentiated a threshold dose of SKF 38393 (3 mg/kg). Locomotion evoked with 5 mg/kg N-n-propyl-N-phenylethyl-p (3-hydroxyphenyl) ethylamine hydrochloride (RU 24213; D2 receptor agonist) was attenuated by HA 966 and MK 801, but not by CPP, CGP 40116 (except at higher doses) or NBQX. SKF 38393 (3 mg/kg) and RU 24213 (5 mg/kg) interacted synergistically to elicit locomotion which was unaffected by CPP, CGP 40116, HA 966 and NBQX, and inhibited by MK 801. (ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Behavioral and biochemical effects of the dopamine D3 receptor-selective ligand, 7-OH-DPAT, in the normal and the reserpine-treated rat.

In normal rats, the dopamine D3 receptor-selective ligand, 7-hydroxy-2-(di-n-propylamino)tetralin (7-OH-DPAT), produced biphasic effects on spontaneous locomotor activity, i.e. suppression at low doses (0.06-0.25 mumol kg-1 s.c.), followed by a gradual increase in motor activity (1.0-4.0 mumol kg-1). The core temperature was decreased at these latter high doses only. The reserpine-induced (8.2 mumol kg-1 s.c.) increase in neostriatal 3,4-dihydroxyphenylalanine (DOPA) accumulation, following treatment with m-hydroxybenzylhydrazine-(NSD-1015) (475 mumol kg-1 i.p.), was dose dependently antagonized by 7-OH-DPAT in the dose range 0.02-4.0 mumol kg-1. The reserpine-induced suppression of spontaneous locomotor activity, however, was antagonized at higher doses only (1.0-4.0 mumol kg-1). Finally, there were no region-selective effects of 7-OH-DPAT on DOPA accumulation in the neostriatum. Thus, it appears that the dopamine D3 receptor-preferring ligand, 7-OH-DPAT, displays the profile of a dopamine D2 receptor agonist, pre- and postsynaptically.

Analysis of Variance↗
PubMed1996

NMDA receptor antagonists increase the release of dopamine in the substantia nigra of reserpine-treated rats.

Microdialysis of the substantia nigra pars reticulata in freely moving rats disclosed a steady release of dopamine and its metabolites which was greatly reduced after reserpine (4 mg/kg s.c.) and alpha-methyl-p-tyrosine (200 mg/kg i.p.) pretreatments. Local infusion of high K+ (100 mM) or L-3,4-dihydroxyphenylalanine (L-DOPA, 10 microM) significantly increased dialysate levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC), but not homovanillic acid (HVA) in this model. Intranigral application of the non-competitive NMDA receptor antagonist dizocilpine (150 nM), or the competitive NMDA receptor antagonist R-DL-(E)-2-amino-4-methyl-5-phosphono-3-pentanoate (CGP 40116, 10 microM), via the dialysis probe, did not affect the release of dopamine or its metabolites in intact rats, but further suppressed these releases in reserpine plus alpha-methyl-p-tyrosine-treated animals. When the same amounts of dizocilpine or CGP 40116 were coinfused with L-DOPA, however, they potentiated the recovery of dopamine 12-24 times, and of DOPAC 5-10 times (but not HVA), as well as producing detectable behavioural arousal. The facilitation of dopamine formation from L-DOPA by NMDA receptor antagonists in the substantia nigra pars reticulata could explain the enhancement of L-DOPA's antiparkinsonian activity by these compounds in behavioural experiments.

2-Amino-5-phosphonovalerate↗
PubMed1991

Detection of neuropeptide Y-like immunoreactivity and messenger RNA in rat platelets: the effects of vinblastine, reserpine, and dexamethasone on NPY expression in blood cells.

Rat plasma contains high basal levels (220 pmol/liter) of neuropeptide Y (NPY)-like immunoreactivity (LI) compared to pig (30 pmol/liter) and man (25 pmol/liter). The platelet-enriched fraction (PEF), obtained from rat blood contained 10,061 pmol/g NPY-LI. However, in human and pig blood, the PEF contained very low levels of NPY-LI. Gradient centrifugation of rat blood showed the highest concentration of NPY-LI (10.8 +/- 0.4 pmol/g) in the platelet fraction. The mononuclear cell fraction contained 1.64 +/- 0.16 pmol/g, whereas only 0.56 +/- 0.06 pmol/g of NPY-LI was found in the red blood cell/polymorphonuclear cell fraction. Characterization of NPY-LI in rat plasma and platelets by high-pressure liquid chromatography showed one predominating peak which coeluted with synthetic NPY (1-36) as well as three minor peaks, one of which coeluted with oxidized NPY. Analysis of NPY messenger RNA (mRNA) in bone marrow of the rat revealed a 0.79-kb-long NPY mRNA. This size is intermediate to the 0.82-kb NPY mRNA in brain and the 0.76-kb NPY mRNA in spleen. The highest level of NPY mRNA in rat blood was found in the mononuclear cell fraction but NPY mRNA was also detected in the platelet fraction. No NPY mRNA was detected in bone marrow or blood from pig and rabbit or from human blood or bone marrow. Forty-eight hours after treatment of rats with vinblastine the content of NPY mRNA and NPY-LI in rat blood was decreased, while the level of NPY-LI in bone marrow was markedly enhanced. Reserpine treatment caused an increase in NPY mRNA content in bone marrow and spleen. After administration of dexamethasone the level of NPY mRNA increased in both spleen and peripheral blood cells with increased NPY-LI content in the spleen. It is concluded that in addition to megakaryocytes in spleen and bone marrow, platelets and possibly also lymphocytes/monocytes in peripheral blood of the rat contain NPY mRNA and peptide. The expression of NPY mRNA in bone marrow, spleen, and blood is influenced by vinblastine, reserpine, and dexamethasone.

Animals↗