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PubMed1982

Effect of reserpine on body temperature in the rat after pretreatment with amphetamine and monoamineoxidase inhibitors.

Intravenous injection of reserpine produced a small but significant hyperthermic effect which is followed by a persistent decrease in temperature. Amphetamine, tranylcypromine and pargyline administered intraperitoneally caused a fall in body temperature. The decrease was higher after pargyline than after amphetamine and tranylcypromine. The initial increase in temperature that was seen immediately after reserpine administration in unanaesthetized and anaesthetized rats was significantly potentiated in the animals pretreated with amphetamine and monoamineoxidase (MAO) inhibitors. The decrease in temperature occurring afterwards is not significantly different from that seen after reserpine alone in conscious rats. However, in anaesthetized rats the hypothermic response was delayed and was not as marked as in conscious animals. The changes in the transient hyperthermic response to reserpine obtained with pretreatment with these drugs are roughly reminiscent of the modification of the effect on blood pressure. In conclusion, the present results confirm that the simple and objective determination of drug induced changes on reserpine effects on temperature may equal the results obtained on blood pressure.

Amphetamine↗
PubMed1994

[Changes in the weight of the uterus, ovaries and adrenal glands in sexually mature rats treated with estradiol and reserpine].

Immature rats of the Wistar strain were used for the experiments. The treatment was administrated on the 35, 36, 37th day after delivery. The animals were divided into 4 groups. The first group received only saline solution, the second group were treated with reserpine, the third group with estradiole, and the forth group with both reserpine and estradiole. The animals were sacrificed on the 38th day after delivery. There was a statistically significant increase in the weight of the uterus and the ovaries after treatment with estradiole alone, and the same was observed for the group treated with reserpine and estradiole. The latter showed less increase in the uterine weight, which might be due to an impairment of estradiole synthesis caused by reserpine. The wight of the adrenal glands of the immature female rats was increased after treatment with estradiole and reserpine. This implies an involvement of the adrenergic system in the interaction between estradiole and testosterone in immature rats.

Adrenal Glands↗
PubMed1994

Effect of nifedipine, a calcium channel inhibitor, on sedation produced by reserpine, clonidine and propranolol in mice.

Spontaneous motor activity, rotarod test and observational rating of sedation were employed to study effect of nifedipine on sedation produced by reserpine, clonidine and propranolol. Reserpine (2 mg kg-1), clonidine (4 mg kg-1), and propranolol (40 mg kg-1) significantly reduced spontaneous motor activity and staying capacity of animals on accelerating rotarod (P < 0.01). Observational sedation was also caused significantly as indicated by a higher score in test. Nifedipine (2 mg kg-1) produced no sedation or excitation on its own. Reduction in spontaneous motor activity produced by reserpine and clonidine was partially reversed in animals treated with nifedipine (P < 0.01). A similar effect of nifedipine was also evident on the observational sedation induced by reserpine and clonidine. Effect of these drugs on rotarod times was nearly totally antagonised by nifedipine. Nifedipine did not oppose the sedation produced by propranolol which actually became significantly greater in the animals pretreated with nifedipine in all three tests. It is concluded that nifedipine antagonizes the sedation produced by reserpine and clonidine, probably by blocking central alpha 2-adrenoceptors. The sedative effect of propranolol can be potentiated by nifedipine possibly because of a pharmacokinetic interaction.

Animals↗
PubMed1996

Muscarinic antagonists microinjected into the subthalamic nucleus decrease muscular rigidity in reserpinized rats.

The ability of anticholinergic agents microinjected into the subthalamic nucleus to reduce reserpine-induced muscular rigidity was assessed in rats. The electromyographical activity of the gastrocnemius-soleus muscle was used as a parameter of muscular rigidity. Reserpine (5 mg/kg i.p.) produced the appearance of electromyographical activity. The muscarinic antagonists M3 (1.27 nmol of 4-DAMP) and M1 (2.36 nmol of pirenzepine) markedly reduced the reserpine-induced electromyographical activity, whereas the M2 antagonist AFDX-116 (2.37 nmol) had no effect. These results suggest that a high cholinergic tone in the subthalamic nucleus is associated with the reserpine-induced muscular rigidity. Moreover, the M3 muscarinic antagonist is more effective than the M1 muscarinic antagonist in reducing the muscular rigidity in reserpinized rats, a model of Parkinson's disease, by blocking the high cholinergic tone in the subthalamic nucleus.

Anesthetics, Intravenous↗
PubMed1976

Colorimetric assay of reserpine in formulations and biological fluids.

Two colorimetric methods are presented for determining reserpine. In the first method, an iron hydroxamate complex is formed through the ester group in position 16 in the reserpine molecule. The color is measured at 535 nm (0.5-6 mg/25 ml). This method is useful for routine and control analyses of reserpine formulations. In the second method the tertiary amino group of reserpine reacts with 2% citric acid in acetic anhydride to form a red-violet complex which is measured at 505 nm (5-400 mug/10 ml). This method could be useful in measuring trace amounts of reserpine present in biological fluids.

Colorimetry↗
PubMed1997

A randomised crossover comparison of reserpine and sustained-release nifedipine in hypertension.

OBJECTIVE: To compare the effectiveness of the combination of hydrochlorothiazide (HCT) plus sustained-release nifedipine with the combination of HCT plus reserpine in lowering high blood pressure (BP) unresponsive to HCT monotherapy. DESIGN: An open, randomised crossover drug trial. SETTING: Outpatients' clinic in Parirenyatwa Hospital, Harare, a tertiary referral centre. SUBJECTS: 32 Black patients of both sexes with newly diagnosed or previously treated hypertension aged between 21 and 65 years who had a BP > 140/95 after receiving HCT 25 mg daily for four weeks were studied. INTERVENTION: Patients were kept on HCT 25 mg daily and were randomised to receive either reserpine 0.25 mg daily or nifedipine (Adalat Retard) 20 mg bd for four weeks. This was followed by a two week washout period during which patients received HCT 25 mg daily only. After the washout period patients were crossed over to the alternative treatment for four weeks. Patients were kept on HCT 25 mg daily throughout the trial. MAIN OUTCOME MEASURES: The main outcome measure was the fall in BP which was taken as the difference between the BP at baseline and the BP at the end of each treatment period. Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) measurements were taken. RESULTS: Both second line drugs were effective in lowering SBP and DBP and there was no significant difference between them. Nifedipine reduced SBP by 18.9 mmHg (95% CI 12.1 to 25.7) and DBP by 9.6 mmHg (95% CI 7.2 to 12.0). Reserpine reduced SBP by 15.9 mmHg (95% CI 8.4 to 23.4) and DBP by 11.1 mmHg (95% CI 7.5 to 14.6). However, only two patients attained the target DBP of < or = 90 mmHg after each active treatment period. CONCLUSION AND RECOMMENDATIONS: Since both agents were equally effective in reducing both SBP and DBP and reserpine is much cheaper than nifedipine, it is recommended that for a developing country like Zimbabwe, the combination of HCT and reserpine at the above doses should be used as the first step to treat mild to moderate hypertension without evidence of end organ damage. However, further trials should compare BP lowering effects as well as end organ protection offered by the trial drugs.

Adult↗
PubMed1982

Bioassay of Reserpine for Possible Carcinogenicity (CAS No. 50-55-5).

A bioassay for possible carcinogenicity of reserpine, an antihypertensive drug for human use, was conducted by administering the test chemical in feed to F344 rats and B6C3F1 mice. Groups of 50 rats and 50 mice of each sex were administered reserpine at two doses, 5 ppm and 10 ppm, for 103 weeks and then observed for an additional 2 weeks. Matched controls consisted of groups of 50 untreated rats and 50 untreated mice of each sex. All surviving animals were killed and necropsied at the end of 104 or 105 weeks. The significant effects that could be related to administration of reserpine at the doses used were decreased body weight and increased tumor formation in dosed male rats and in mice of both sexes. Dosed male rats had an increased incidence of adrenal medullary pheochromocytomas. Among dosed mice, some males developed undifferentiatedcarcinomas of the seminal vesicles, which rarely occur in control mice, and females had an increased incidence of mammary cancer. It was concluded that, under the conditions of the bioassay, reserpine was carcinogenic in male rats and in mice of both sexes, producing three different kinds of cancers. reserpine was not carcinogenic for female rats, but they may not have received a high enough dose for maximum test sensitivity. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Negative Male Mice: Positive Female Mice: Positive

Journal Article↗
PubMed1997

Quantitative ionspray liquid chromatographic/tandem mass spectrometric determination of reserpine in equine plasma.

A method based on ionspray liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed for the determination of reserpine in equine plasma. A comparison was made of the isolation of reserpine from plasma by liquid-liquid extraction and by solid-phase extraction. A structural analog, rescinnamine, was used as the internal standard. The reconstituted extracts were analyzed by ionspray LC/MS/MS in the selected reaction monitoring (SRM) mode. The calibration graph for reserpine extracted from equine plasma obtained using liquid-liquid extraction was linear from 10 to 5000 pg ml-1 and that using solid-phase extraction from 100 to 5000 pg ml-1. The lower level of quantitation (LLQ) using liquid-liquid and solid-phase extraction was 50 and 200 pg ml-1, respectively. The lower level of detection for reserpine by LC/MS/MS was 10 pg ml-1. The intra-assay accuracy did not exceed 13% for liquid-liquid and 12% for solid-phase extraction. The recoveries for the LLQ were 68% for liquid-liquid and 58% for solid-phase extraction.

Animals↗
PubMed1997

Effect of reserpine-induced depletion of synaptic dopamine on [11C]raclopride binding to D2-dopamine receptors in the monkey brain.

Positron emission tomography was used to examine the in vivo binding of [11C]raclopride to D2-dopamine (DA) receptors in the striatum of two Cynomolgus monkeys after a single dose of reserpine (1 mg/kg, i.v.). A Scatchard procedure was repeated five times to follow D2 receptor density and apparent affinity for 7 weeks after reserpine. Reserpine-induced depletion of DA lead to a marked increase in [11C]raclopride binding, which was still detectable 20 days after treatment. Scatchard analyses indicated that the measured increase in [11C]raclopride binding reflected an increase in receptor affinity but no evident change in receptor density (Bmax). Thus, the increase in [11C]raclopride binding after reserpine should correspond to a reduced competition with endogenous DA for binding to D2 receptors. The results were used to estimate the DA-induced D2 occupancy to be about 40% at physiological conditions.

Animals↗
PubMed2003

Effects of CB1 cannabinoid receptor modulating compounds on the hyperkinesia induced by high-dose levodopa in the reserpine-treated rat model of Parkinson's disease.

The present study was designed to determine the potential of CB1 cannabinoid receptor modulating compounds in the treatment of L-3,4-dihydroxyphenylalanine (L-dopa)-induced dyskinesia in Parkinson's disease. In the reserpine-treated rat model of parkinsonism, administration of a high dose of L-dopa (150 mg/kg) but not of Cl-APB (0.5 mg/kg) or quinpirole (0.5 mg/kg) produced a hyperkinetic state characterised by an increase in horizontal and vertical activity, which likely represent correlates of antiparkinsonian and dyskinetic activity, respectively. Injection of the CB1 cannabinoid receptor antagonist SR141716 (0.1-3 mg/kg) reduced the increase in vertical activity elicited by L-dopa without affecting the increase in horizontal activity. Injection of the CB1 cannabinoid receptor agonist WIN55,212-2 (0.1-3 mg/kg) reduced the L-dopa-induced increase in vertical activity and, at the highest dose only (3 mg/kg), also reduced horizontal activity elicited by L-dopa. WIN55,212-2 (1 mg/kg) reduced motor activity induced by both the D1 receptor agonist Cl-APB (0.5 mg/kg) and the D2 receptor agonist quinpirole (0.5 mg/kg) in the reserpine-treated rat. SR141716 (1 mg/kg) had no effects on motor activity induced by Cl-APB (0.5 mg/kg) nor quinpirole (0.5 mg/kg) in the reserpine-treated rat. Injection of the inhibitor of endocannabinoid transport AM404 (0.1-1 mg/kg) did not affect the increase in horizontal or vertical activity elicited by L-dopa (150 mg/kg) in the reserpine-treated rat. The data suggest that both CB1 cannabinoid receptor antagonists and agonists can modulate the behavioural effects of L-dopa and may be useful for the treatment of the dyskinesia associated with long-term L-dopa treatment of Parkinson's disease.

Adrenergic Uptake Inhibitors↗
PubMed2001

Early changes in neuropeptide mRNA expression in the striatum following reserpine treatment.

Chronic dopamine depletion produces neurochemical changes within the striatum as well as enhanced behavioral and metabolic responses to dopamine agonists. Changes in striatal neuropeptides have been consistently described, including increased expression of preproenkephalin mRNA and decreased expression of preprotachykinin and prodynorphin mRNA. Acute dopamine depletion following treatment with reserpine also produces enhanced behavioral and metabolic responses to agonist treatment which develop rapidly. In the present study, we used in situ hybridization histochemistry to investigate whether acute neurochemical changes occur following reserpine treatment. We evaluated neuropeptide mRNA expression in the striatum and nucleus accumbens at several time points from 6 to 120 h following single doses of reserpine and AMPT. The aim of these studies was to determine if changes in neuropeptide mRNA expression occur following acute dopamine depletion and whether such changes are specific to the striatum. Changes in striatal neuropeptide mRNA expression developed rapidly. Preproenkephalin mRNA expression by striatopallidal neurons was unchanged at 48 h, but increased by 44% at 120 h. Preprotachykinin mRNA expression in striatonigral neurons was increased at 6 h and then fell, with a maximal decrease of 45% at 48 h and partial recovery by 120 h. Prodynorphin mRNA expression was unchanged. Expression of preproenkephalin and preprotachykinin mRNA was also examined in subregions of the striatum and the nucleus accumbens. Expression of preproenkephalin mRNA was uniform in the striatum and higher in the core than the shell of the nucleus accumbens. Preprotachykinin mRNA expression in the striatum was higher in the lateral quadrants and was higher in the shell than in the core of the nucleus accumbens. The changes in neuropeptide mRNA following treatment with reserpine were only found in the striatum. These data provide further evidence for early alterations in neuronal function in the striatum following acute dopamine depletion and suggest that neuropeptide expression by striatonigral neurons may be more rapidly regulated in response to changes in dopamine levels.

Adrenergic Uptake Inhibitors↗
PubMed1988

The mode of action of bromocriptine following pretreatment with reserpine and alpha-methyl-p-tyrosine in rats.

The ability of bromocriptine (BRC), a selective dopamine D-2 receptor agonist, to induce yawning responses was studied in rats pretreated with reserpine and alpha-methyl-p-tyrosine (alpha-MPT). BRC (1 20 mg/kg IP) evoked yawning responses, which were pronounced at 2.5 mg/kg and characterized by the head moving downward. Higher doses of BRC (5 20 mg/kg) dose-dependently delayed the onset and peak time of yawning. A low dose of the selective D-1 dopamine receptor agonist SK&F38393 did not induce yawning but enhanced the BRC-induced response. Pretreatment with reserpine (1 and 5 mg/kg SC), alpha-MPT (100 and 300 mg/kg IP) and reserpine (1 mg/kg) plus alpha-MPT (100 mg/kg) was able to significantly reduce BRC-induced yawning. The inhibitory effects were prevented by a low dose of SK&F38393 (0.5 mg/kg IP). In particular, combined treatment with reserpine (5 mg/kg) and BRC (10 and 20 mg/kg) elicited upright fighting and jumping behaviors which were inhibited by haloperidol (1 mg/kg IP), a non-selective D-1 and D-2 receptor antagonist, SCH23390 (0.05 mg/kg SC). a selective D-1 receptor antagonist, or sulpiride (20 mg/kg IP), a potent D-2 receptor antagonist, and were potentiated by SK&F38393 (0.5 mg/kg). SCH23390 (0.05 mg/kg) decreased BRC-induced yawning and the apomorphine (low doses)-induced potentiation of BRC yawning, and prevented the apomorphine (high doses)-induced reduction of BRC yawning. SCH23390 also inhibited apomorphine-induced stereotypy and BRC-induced potentiation of apomorphine stereotypy.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1985

Reserpine inhibits release of vasopressin from the neural lobe of the pituitary in dehydrated rats.

The effects of reserpine on the osmotically induced release of pituitary vasopressin were studied (i) by measuring the urinary excretion and the vasopressin content of the neural lobe of pituitary, and (ii) by examining the ultrastructural morphology of axons in the neural lobe of dehydrated rats. After water deprivation for two days, control rats displayed characteristic antidiuretic response including a 75% reduction of urinary excretion and a six-fold decrease in vasopressin content of the neural lobe associated with a dramatic depletion of neurosecretory granules in corresponding axons. In contrast, when they received two dialy injections of reserpine, animals dehydrated for two days showed both urinary excretion and vasopressin contents in the neural lobe that remained at levels comparable to those measured in the normally hydrated rats. Additionally, neural-lobe axons of such dehydrated, reserpine-treated rats displayed a normal amount of neurosecretory granules. These data indicate that reserpine inhibits release of vasopressin from the neural lobe and favour the concept of a facilitatory role of the catecholaminergic innervation in the control of hypothalamo-neurohypophysial vasopressin-secreting neurons.

Animals↗
PubMed1994

Effect of reserpine on 5-hydroxytryptophan (5HTP)-immunoreactive neurons in the rat brain.

By immunohistochemistry of rat brain in conjunction with a specific antibody against 5-hydroxytryptophan (5HTP), we examined immunoreactivity to 5HTP in neurons, from which 5-hydroxytryptamine (5HT; serotonin) was depleted by reserpine treatment. The distribution patterns of 5HTP-positive neurons overlapped with those of 5HT neurons. Treatment with reserpine (5 mg/kg, 90 min before death) caused a complete suppression of 5HT-positive staining, but 5HTP-immunostaining remained in perikarya of the nuclei raphe dorsalis, centralis superior and obscurus. Treatment with reserpine (25 mg/kg, 90 min before death) suppressed the 5HTP-immunoreaction in certain perikarya (e.g. of the nucleus raphe dorsalis) and fibres; however, 5HTP-immunostaining remained in perikarya of the nuclei centralis superior and raphe obscurus. This suggests that these neurons synthesize more 5HTP by a process which appears to be stimulated by reserpine.

5-Hydroxytryptophan↗
PubMed1981

Antagonism of reserpine rigidity without inducing sedation.

The effects of pretreatment with chlorpromazine, promethazine or SKF 7265 on the severity of reserpine-induced rigidity were evaluated using a series of behavioral responses. Chlorpromazine (10 mg/kg) reduced the severity of the syndrome, particularly the tremor, but only at doses that also produced marked sedation. SKF 7265 was more effective than chlorpromazine and produced no detectable sedation or other motor impairment. Promethazine was ineffective in protecting against the effects of reserpine. These studies demonstrate that motor and behavioral abnormalities induced by high doses of reserpine can be blocked without inducing generalized sedation. This would suggest that it is possible to separate pharmacologically the motor pathways responsible for reserpine rigidity and those responsible for sedation.

Acridines↗
PubMed1977

The influence of temperature upon reserpine-induced supersensitivity of guinea-pig isolated atria to isoprenaline and salbutamol.

1. The aim of this investigation was to determine whether supersensitivity of isolated atria to sympathomimetic amines following pretreatment with reserpine was evident at low temperatures, which alone induced supersensitivity. 2. Cumulative dose-response curves for the positive inotropic and chronotropic responses of isolated guinea-pig atria to isoprenaline and the partial agonist salbutamol were plotted as a percentage of the maximum response to isoprenaline. 3. In atria from reserpine-pretreated guinea-pigs set up at 38 degrees C, supersensitivity of both rate and tension responses was observed as a shift of the curves to the left and an increase of the maximum responses to salbutamol. Tension responses were potentiated more than rate responses. At 30 degrees C the supersensitivity became less apparent and at 25 degrees C was virtually absent. 4. The dose-response curves in untreated atria at low temperatures revealed that hypothermia itself produced supersensitivity of rate and tension responses. The dose-response curves were displaced to the left and the salbutamol maxima were raised so that at 25 degrees C it became almost a full agonist. The hypothermia-induced supersensitivity was therefore sufficient to mask any supersensitivity resulting from pretreatment with reserpine. 5. The hypothermia-induced supersensitivity of the rate response was dependent upon the method of plotting. When plotted in absolute units of beats per min no supersensitivity of the rate response was evident. Supersensitivity of the tension response at the lower temperatures and of both rate and tension responses following pretreatment with reserpine were independent of the plotting method.

Albuterol↗
PubMed1985

Amphetamine induced release of endogenous dopamine in vitro is not reduced following pretreatment with reserpine.

The release of endogenous dopamine evoked by electrical stimulation or by exposure to (+)-amphetamine (10 microM) was determined in superfused striatal slices of the rat. The spontaneous and the electrically-evoked release of dopamine were significantly increased in the presence of nomifensine (10 microM). After reserpine pretreatment (5 mg/kg, s.c., 24 h), the striatal dopamine content was reduced by about 90%. Exposure to 10 microM (+)-amphetamine during 2 min released similar amounts of dopamine from striatal slices of untreated or reserpine pretreated rats. Similar results were obtained when monoamine oxidase activity was inhibited in vivo with pargyline. Pretreatment with reserpine does not modify the (+)-amphetamine-induced release of dopamine, in spite of the marked reduction of the striatal dopamine content. These results provide direct evidence for the view that (+)-amphetamine releases dopamine from a special, reserpine-resistant pool of newly synthetized transmitter.

Animals↗
PubMed1986

Reversal of the reserpine-induced ptosis by L-threo-3,4-dihydroxy-phenylserine (L-threo-DOPS), a (-)-norepinephrine precursor, and its potentiation by imipramine or nialamide.

The effect of L-threo-DOPS on the reserpine-induced ptosis in mice and its modification by imipramine, a norepinephrine (NE) uptake inhibitor, or nialamide, a monoamineoxidase inhibitor, were studied. Intraperitoneal (i.p.) injection of L-threo-DOPS (800 mg/kg) significantly reduced the severity of the ptosis. This reversal of the ptosis by L-threo-DOPS was markedly potentiated by i.p. injection of either imipramine (2.5 mg/kg) or nialamide (30 mg/kg). Response to L-threo-DOPS was also significantly potentiated by intracerebroventricular (i.c.v.) injection of imipramine (10 micrograms). On the other hand, this treatment with imipramine (10 micrograms, i.c.v.) also significantly potentiated the reversal of the ptosis by NE (20 micrograms, i.c.v.), but the reversal by the subcutaneous (s.c.) injection of NE (1 and 3 mg/kg) was not affected. Reserpine (5 mg/kg, i.p.) markedly decreased the brain content of NE in mice, whereas L-threo-DOPS (400 mg/kg, i.p.) slightly restored it. Moreover, by the pretreatment with nialamide (30 mg/kg, i.p.), L-threo-DOPS produced a significant increase in the brain content of NE in reserpine-treated mice. These results suggested that L-threo-DOPS was capable of reversing the reserpine-induced ptosis due to the formation, at least in part of (-)-NE at the synaptic sites of central noradrenergic neurons.

Animals↗