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PubMed1988

Nonspecific supersensitivity induced by reserpine in guinea pig cardiac ventricle tissue.

The depletion of norepinephrine stores by chronic reserpine pretreatment is thought to be responsible for the development of supersensitivity in cardiac tissue. The present study was designed to determine if reserpine-induced supersensitivity could be demonstrated in isolated guinea pig right ventricular strips, if it was associated with beta adrenoceptor proliferation and was specific for beta adrenoceptor agonists. In addition, reserpine dose-dependency of the phenomenon was tested for by using two pretreatment regimens to determine if supersensitivity was the result of direct or possibly toxic effects of reserpine. Pretreatment of guinea pigs with reserpine (0.1 mg/kg/day) for 7 days resulted in over 90% depletion of cardiac norepinephrine stores. Supersensitivity to the inotropic effects of isoproterenol, impromidine and forskolin was demonstrated. Associated with the supersensitivity was a significant increase in beta adrenoceptor density. Muscarinic receptor density was actually decreased. This pretreatment regimen also was associated with a significant (30%) drop in body weight suggesting that the phenomenon might be the result of a direct toxic effect of reserpine. Pretreatment of guinea pigs with a lower dose of reserpine (0.03 mg/kg/day) for 7 days produced the same degree of norepinephrine depletion, nonspecific inotropic supersensitivity and beta adrenoceptor proliferation in the absence of a significant reduction in body weight. The degree of supersensitivity induced by the two pretreatment regimens was between 2- to 3-fold for all three agonists tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Dissociation between acid secretion and mucosal blood flow after treatment of rats with reserpine.

The correlation between acid secretion and mucosal blood flow in the gastric mucosa after administration of reserpine to rats was determined in an attempt to define the etiology of reserpine-induced gastric erosions. Although gastric acid output was increased gradually by administration of reserpine, mucosal blood flow was not significantly affected. The increase in acid output induced by reserpine was completely prevented by pretreatment with atropine. Reserpine-induced increase in acid secretion may have been mediated by the vagus nerves, probably as a result of central and/or peripheral diminution in noradrenergic inhibitory mechanisms. The dissociation between mucosal blood flow and acid secretion, resulting in a relative ischemic state in the gastric mucosa, may have occurred in part from reduced cardiac function after treatment with reserpine. Vagal stimulation induced a parallel increase in both acid secretion and mucosal blood flow in control rats. 6-Hydroxydopamine-induced sympathectomy did not increase mucosal blood flow to a degree corresponding to the increase in acid output by vagal stimulation. In animals treated with 6-hydroxydopamine, gastric erosions occurred. We conclude that reserpine increases acid output but without a parallel increase in the mucosal blood flow and that the erosions which occur are probably due to the relative ischemic state of the gastric mucosa.

Animals↗
PubMed1986

Stability of reserpine injections and tablets submitted by U.S. hospitals.

The stability of reserpine injections and tablets that had been stored in hospital pharmacies across the United States was studied. Through a voluntary FDA drug stability program, all hospital pharmacies in the United States were asked to complete a response card indicating information about the reserpine injections and tablets they had in stock. Based on the responses, FDA selected 93 samples of reserpine injections and 51 samples of reserpine tablets. The samples of injections were subjected to tests for identification, pH, presence of other alkaloids, presence of 3,4-dehydroreserpine, and strength. All samples of reserpine injections met USP requirements. Two samples of reserpine tablets representing one lot each from two manufacturers failed to meet USP requirements for content uniformity. Reserpine injections and tablets appear to be stable under actual marketplace conditions.

Chromatography, High Pressure Liquid↗
PubMed1982

Effect of reserpine pretreatment on mechanical responsiveness and [125I]Iodohydroxybenzylpindolol binding sites in the guinea-pig right atrium.

The inotropic and chronotropic responses of the guinea-pig right atrium to several pharmacologic agents were measured after acute (0.1 mg/kg/day x 1) and chronic (0.1 mg/kg/day x 7) reserpine administration. A small increase in the sensitivity of the pacemaker to isoproterenol occurred after acute reserpine treatment which was followed by a much greater change in sensitivity to the beta agonist when pretreatment was extended for 7 days. Chronotropic responsiveness to calcium, histamine and pilocarpine was not altered by reserpine pretreatment. The acute administration of reserpine resulted in a slight inotropic supersensitivity of paced right atria to isoproterenol, calcium and histamine. Pretreatment for 7 days produced an additional increase in inotropic sensitivity to isoproterenol but did not affect contractile responses to the other agents. The catecholamine-specific nature of the supersensitivity induced by chronic reserpine treatment suggested that a change in the number and/or affinity of beta adrenergic receptors was involved. The radiolabeled beta adrenoceptor antagonist [125]iodohydroxybenzylpindolol (I-HYP) was used to test this hypothesis. Preliminary experiments revealed the presence of a single class of noninteracting (nH = 0.99), high affinity (Kd = 100 pM) binding sites which exhibited stereospecificity and saturability (47.2 fmol/mg of protein). The agonist potency series for the inhibition of I-HYP binding was identical to the series for mediating mechanical responses. Taken collectively this information suggests that the high affinity I-HYP binding site in the guinea-pig right atrium represents the beta adrenergic receptor. As determined by Scatchard analyses, neither acute (1-day) nor chronic (7-day) low-dose (0.1 mg/kg/day) reserpine administration altered the number or affinity of I-HYP binding sites. It is concluded that changes in beta receptor characteristics are not responsible for reserpine-induced supersensitivity in this tissue.

Aminophylline↗
PubMed1983

Cellular energy systems and reserpine ulcer in rats.

Gastric ulcer was elicited in rats by reserpine (5 mg x kg-1 sc.) administration. Ulcer formation (number and severity) was measured 6, 12, 18 and 24 hr after reserpine administration. At the time of killing of the animals, tissue levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), cyclic adenosine monophosphate (cAMP) were measured enzymatically and by radioimmunoassay in the gastric fundal mucosa. The sum of ATP + ADP + AMP (adenylate pool) and the ratio of ATP x ADP-1 were calculated. It was found that (1) the tissue levels of ATP, AMP, cAMP, sum of ATP / ADP + AMP (adenylate pool) and ratio of ATP x ADP-1 increased significantly in the gastric fundal mucosa 6 hr after reserpine administration, thereafter these values decreased gradually and significantly; (2) the tissue level of ADP increased significantly in the gastric fundal mucosa 6 hr after reserpine administration, meanwhile its level increased significantly at 18 and 24 hr; (3) the value of energy charge (ATP + 0.5 ADP x ATP + ADP + AMP-1) remained unchanged; (4) the peaks of biochemical alterations in the gastric fundus mucosa preceded he appearance of ulcers. It was concluded that (1) reserpine ulcer appears after an active metabolic response in the rat gastric fundal mucosa; (2) hypoxaemic damage in the gastric fundal mucosa can be excluded as a possible underlying mechanism of ulcer formation produced by reserpine administration; (3) before the appearance of reserpine ulcer, significant changes in the feedback mechanism, system, i.e. between the ATP--membrane ATPase--ADP and the ATP--adenylate cyclase--cAMP energy systems, can be observed in the rat gastric fundal mucosa.

Adenosine Diphosphate↗
PubMed1976

Monoamine oxidase inhibition and the induction of ponto-geniculo-occipital wave activity by reserpine in the cat.

Reserpine induces ponto-geniculo-occipital wave activity similar to that seen in the cat during the rapid eye movement phase of sleep. This action of reserpine was blocked by the monoamine oxidase inhibitors, pheniprazine, harmaline and clorgyline, but not deprenyl or its demethylated analog. After a single dose (20 mg/kg) of either pheniprazine or harmaline, the time course of antagonism of the effect of reserpine was in good correspondence with inhibition of monoamine oxidase but not with restoration of the serotonin content of several regions of the brain. Harmaline had a reversible effect while that of pheniprazine persisted for weeks. Clorgyline in low doses (0.5-1.0 mg/kg), at which it is a specific inhibitor of type A monoamine oxidase, antagonized the action of reserpine for over 2 weeks. Deprenyl and its demethylated analog failed to suppress the reserpine-induced waves even at 10 times the dose of clorgyline when they should have completely inhibited type B monoamine oxidase. In contrast to antagonism of reserpine, suppression of rapid eye movement sleep by these monoamine oxidase inhibitors could be temporally dissociated from their inhibition of the enzyme. It is concluded that suppression of the induction of ponto-geniculo-occipital waves by reserpine after administration of the monoamine oxidase inhibitors is a specific effect of these drugs and is related to inhibition of type A monoamine oxidase. Suppression of rapid eye movement sleep is probably a nonspecific effect and not related to inhibition of the enzyme.

Animals↗
PubMedDate not supplied

[Treatment of Cushing's syndrome with large doses of reserpine].

The effectiveness of high doses of reserpine was studied in two groups of patients, suffering from Icenko-Cushing's disease. The patients of the first group received gamma-beam therapy combined with high doses of reserpine. The patients of the second group were treated with gamma-beam radiation associated with unilateral adrenalectomy plus high doses of reserpine. The controls were treated as described above, but without reserpine use. The results obtained have shown that reserpine monotherapy is not recommended in Icenko-Cushing's disease. High doses of reserpine combined with gamma-beam radiation alone or coupled with unilateral adrenalectomy shortened the period of the appearance of remission. The arterial blood pressure was significantly lower in patients treated with high doses of reserpine.

Adolescent↗
PubMed1981

Comparison of reserpine-induced supersensitivity of newborn and adult rabbit ventricular muscles to cardiotonic agents.

The myocardium of the neonate has incomplete sympathetic innervation and decreased sensitivity to cardiotonic agents. It is not known whether the neonatal myocardium exhibits the tendency to develop reserpine-induced supersensitivity to cardiotonic agents. Using isolated ventricular muscles from 1-week-old and adult rabbits, concentration-response relationships of inotropic tension to isoproterenol, ouabain, norepinephrine and calcium were determined with and without reserpine pretreatment. Ventricular muscles from the newborn animals exhibited the same degree of reserpine-induced supersensitivity to isoproterenol and ouabain as that seen in the adult animals. Although the newborn demonstrated reserpine-induced supersensitivity to calcium, the adult did not. Neither age group demonstrated reserpine-induced supersensitivity to norepinephrine. These findings indicate that newborn animals are capable of producing reserpine-induced supersensitivity, despite the immaturity of their cardiac sympathetic innervation, contractile machinery and beta-adrenergic mechanisms. These results also indicate the non-selective nature of reserpine-induced supersensitivity.

Animals↗
PubMed1995

Effects of reserpine on extracellular caudate dopamine and hippocampus norepinephrine responses to amphetamine and cocaine: mechanistic and behavioral considerations.

Following reserpine pretreatment to disrupt vesicular stores of dopamine and norepinephrine, in vivo microdialysis was used in behaving rats to evaluate the role of vesicles in the neurochemical and behavioral responses to amphetamine and cocaine. Reserpine (2.5 mg/kg, 24 hr) completely prevented the hippocampus norepinephrine responses to 20 mg/kg of cocaine and to 0.5, 1.25 and 5.0 mg/kg of amphetamine. Likewise, reserpine almost completely abolished the caudate putamen dopamine response to cocaine. In contrast, the effect of reserpine on the amphetamine-induced dopamine response varied as a function of amphetamine dose. Although the dopamine response to 1.25 mg/kg of amphetamine was unchanged by reserpine pretreatment, the dopamine responses to both the lowest (0.5 mg/kg) and highest (5.0 mg/kg) doses of amphetamine were significantly attenuated by about 65% and 50%, respectively. These results indicate that the norepinephrine response to amphetamine is dependent on vesicular stores of transmitter at all doses of the drug. However, although amphetamine can release dopamine from a reserpine-resistant (non-vesicular) pool, it also appears that this response partially depends on vesicular stores, especially at low and high doses of drug. Concomitant behavioral assessments revealed that the behavioral responses to cocaine and the lowest dose of amphetamine, like the dopamine responses, were significantly suppressed by reserpine pretreatment. In contrast, at the intermediate dose of amphetamine, stereotypies were significantly enhanced. These altered behavioral profiles are discussed in terms of a balance between increases in both dopamine and norepinephrine produced by amphetamine.

Amphetamine↗
PubMed1993

Reserpine binding to a vesicular amine transporter expressed in Chinese hamster ovary fibroblasts.

The potent antihypertensive drug reserpine inhibits the transport of biogenic amines into adrenal chromaffin granules and synaptic vesicles. Reserpine acts by binding almost irreversibly to the vesicular amine transporter, and this interaction has been used both to study the mechanism of transport and to purify the protein responsible. Recent isolation of a cDNA for the rat chromaffin granule amine transporter (CGAT) by selection in the neurotoxin 1-methyl-4-phenylpyridinium now permits an analysis of the interaction with reserpine at a molecular level. Using membranes from stable transformants expressing the transporter, we show that reserpine binds specifically and quantitatively to CGAT. As with the native protein in bovine chromaffin granules, a pH gradient accelerates reserpine binding, and amine substrates compete for binding with reserpine. However, 1-methyl-4-phenylpyridinium and tetrabenazine, the other principal inhibitor of vesicular amine transport, compete very poorly with reserpine for binding, suggesting that they interact with CGAT at distinct sites.

1-Methyl-4-phenylpyridinium↗
PubMedDate not supplied

Determination of reserpine and rescinnamine in Rauwolfia serpentina powders and tablets: collaborative study.

A liquid chromatographic (LC) method for determining reserpine and rescinnamine in Rauwolfia serpentine powders and tablets, which uses fluorescence detection, was subjected to a collaborative study. The procedure for extraction and purification is a simplified version of that used in the current official method for analysis of these products. LC separations are performed on a normal-phase column. The mobile phase is methanol to which a small volume of an aqueous solution of 1-pentanesulfonic acid sodium salt can be added to achieve desired elution characteristics. Reserpine and rescinnamine elute at approximately the same time but can be individually quantitated by appropriate settings of the fluorescence detector. Reserpine is determined at an excitation wavelength of 280 nm and an emission wavelength of 360 nm, because rescinnamine is completely non-fluorescent at these wavelengths. Rescinnamine is determined at an excitation wavelength of 330 nm and an emission wavelength of 435 nm, because reserpine is completely nonfluorescent at these wavelengths. The following materials were used for the study: one sample of United States Pharmacopeia (USP) standard R. serpentine powder, one tablet type labeled as containing 100 mg R. serpentine and 2 tablet types labeled as containing 50 mg R. serpentine. For each of the 4 materials, 2 pairs of blind duplicates were prepared. Three materials were analyzed in duplicate by 8 laboratories. One of the 2 tablets labeled to contain 50 mg R. serpentine was analyzed only by 7 of 8 participating laboratories. Average combined content of reserpine and rescinnamine was 0.144% for the USP raw material and 0.132, 0.135, and 0.137% for the 3 commercial tablets. Reproducibility relative standard deviation values were 5.72, 5.93, 8.61, and 3.48% and repeatability relative standard deviation values were 2.57, 4.87, 3.19, and 1.99% for the 4 samples. The Associate Referee conducted a study to determine recoveries of reserpine plus rescinnamine by this method from mixtures simulating sample extracts. Average recovery of 15 determinations was 100.1%, with a relative standard deviation of 1.3%. The LC method for determination of reserpine and rescinnamine in R. serpentine powders and tablets has been adopted first action by AOAC INTERNATIONAL.

Chromatography, Liquid↗
PubMed2006

Pre- and postsynaptic actions of a partial D2 receptor agonist in reserpinized young rats: longevity of agonistic effects.

Partial D2 receptor agonists (e.g., terguride, preclamol, and aripiprazole) have antagonist-like effects at normosensitive D2 postsynaptic receptors and synthesis modulating autoreceptors. In reserpine-pretreated adult and young rats, however, partial D2 agonists function like high efficacy agonists at D2 postsynaptic receptors and autoreceptors (i.e., terguride increases locomotor activity and decreases dopamine synthesis). The purpose of the present study was to examine the time-course of these pharmacological effects. In all experiments, preweanling rats were given daily injections of reserpine (1 mg/kg, i.p.) or vehicle on postnatal day (PD) 16-PD 20. In the dopamine synthesis experiments, the ability of terguride (0.8 mg/kg) to reduce striatal DOPA accumulation (in NSD-1015 treated rats) was assessed either 5 h or 1, 2, 4, or 8 days (Experiment 1) or 4, 8, 12, 16, 20, or 24 days (Experiment 2) after reserpine pretreatment. In the behavioral experiments, locomotor activity of vehicle or terguride (0.8 mg/kg, i.p.) treated rats was assessed 5 h or 1, 2, 4, or 8 days after the 5-day reserpine regimen. Results from the dopamine synthesis experiments showed that terguride caused agonist-like effects (i.e., decreased DOPA accumulation) at only the 5 h and 1 day time points, although terguride did not induce its normal antagonist-like effects even 20 days after reserpine pretreatment. In the behavioral experiments, terguride stimulated locomotor activity for only the initial 2 days after reserpine pretreatment. The results of the present study show that the agonistic effects of terguride at pre- and postsynaptic receptors are short-lived, but terguride may not exhibit normal antagonistic effects, at least at synthesis modulating autoreceptors, until long after conclusion of reserpine pretreatment.

Age Factors↗
PubMed1963

THE EFFECT OF INTRA(CEREBRO)VENTRICULAR RESERPINE ON THE ACETYLCHOLINE CONTENT OF THE HEART, ILEUM AND HYPOTHALAMUS OF THE DOG.

The effect of injection of reserpine into the cerebral ventricles on the acetylcholine contents of the sino-atrial node, ileum and hypothalamus of the dog was studied in ten dogs. Another group of five dogs served as a control. The effect of intravenous administration of reserpine, in the same dose as given intracerebroventricularly, was also studied on the acetylcholine content of these tissues in five dogs. General sedation, bradycardia, miosis, salivation, emesis and purgation were looked for. Tissues were removed 1 hr after administration of reserpine for estimation of acetylcholine content, which was increased in all the tissues studied. The increase in the peripheral tissues was greater than in the hypothalamus. The increase in the acetylcholine content was not quantitatively related to the other effects of reserpine. The increase in the acetylcholine content of the sino-atrial node and the ileum and also the peripheral effects observed on intracerebroventricular administration of reserpine can be attributed to its central action. With the same dose of reserpine given intravenously the acetylcholine content of the sino-atrial node was significantly increased, while that of the hypothalamus and ileum was not.

Acetylcholine↗
PubMed1996

Reserpine-induced increases in neuropeptide Y mRNA of guinea pig sympathetic ganglia using in situ hybridization.

BACKGROUND: Neuropeptide Y (NPY) is synthesized in sympathetic ganglia by specific mRNA, to which rat probes are currently available. In the rat model, reserpine treatment increases NPY mRNA through a mechanism involving enhanced preganglionic activity. Probes for NPY mRNA have been used exclusively in rat models. In this study, we assessed whether a rat NPY cRNA probe could be used to index reserpine-induced changes in NPY mRNA levels of sympathetic ganglia in the guinea pig. METHODS: Guinea pigs were given vehicle or reserpine pretreatment. In situ hybridization for NPY mRNA was done on the superior cervical and stellate ganglia of four control and four reserpine-treated rats. Autoradiographic density was digitized using an automated image analysis system. RESULTS: Following in situ hybridization of tissue sections, autoradiographic density of specific NPY mRNA binding was evident in nerve cell bodies in the superior cervical and stellate ganglia. Reserpine pretreatment was associated with an increase in NPY mRNA levels in both types of ganglia. CONCLUSION: These results indicate that reserpine treatment in the guinea pig produces increased neuronal NPY mRNA levels. The study also showed that rat NPY cRNA probe can be used to quantify alterations in NPY mRNA levels in the guinea pig.

Animals↗
PubMed1988

Reciprocal changes in striatal dopamine and beta-phenylethylamine induced by reserpine in the presence of monoamine oxidase inhibitors.

Recent studies have demonstrated that selective monoamine oxidase inhibition may induce changes in brain beta-phenylethylamine availability following lesions. The present study used this approach to re-assess the possible effects of reserpine on striatal concentrations of beta-phenylethylamine and of other amines and selected metabolites. Mice were injected with pargyline (2,200 mg kg-1, 4 h), clorgyline (2 mg kg-1, 2 h) or (-)deprenyl (2 mg kg-1, 2 h) alone or in combination with reserpine (1, 10 mg kg-1, 2 h). Increases in beta-phenylethylamine accumulation were observed in the presence of both (-)deprenyl or pargyline respectively after reserpine except in the case of combined 200 mg kg-1 of pargyline plus 1 mg kg-1 of reserpine. In this condition, a minimal dopamine decrease was observed (to 80% of the concentration of pargyline-treated controls). Increases in beta-phenylethylamine concentration were not observed with reserpine alone (1 or 10 mg kg-1). In the latter condition, the concentrations of beta-phenylethylamine remained at control values due to the activity of monoamine oxidase B. Changes in p-tyrosine, 5-hydroxytryptamine or tryptophan did not consistently accompany increases in beta-phenylethylamine accumulation. Increased beta-phenylethylamine accumulation was always accompanied by the decreases in dopamine induced by reserpine in mice with either non-selective (200 mg kkg-1 pargyline) or type B monoamine oxidase inhibition (2 mg kg-1 pargyline or deprenyl). These data suggest that although the changes in beta-phenylethylamine accumulation may not be due simply to p-tyrosine availability they are related to dopamine levels in the intact striatum.

Animals↗
PubMed1987

Cardiac alpha- and beta-adrenoceptor sensitivity and binding characteristics after chronic reserpine pretreatment.

Cardiac alpha- and beta-adrenoceptor sensitivities were examined after chronic pretreatment of rats with reserpine. Increases in sensitivity would indicate that the receptor is under the influence of the sympathetic innervation, removal by catecholamine depletion with reserpine of the tonic effect of neurotransmitter release would permit receptor upregulation. The positive inotropic responses of paced left atria and papillary muscles and the positive chronotropic responses of spontaneously beating right atria were recorded. A concentration-response curve to isoprenaline (beta-adrenoceptor-mediated) was followed, in the presence of beta-blockade, by one to methoxamine (alpha-adrenoceptor-mediated). Methoxamine exerted positive inotropy of left atria and papillary muscles, the maxima being 43.2 +/- 2.7 and 26.8 +/- 4.4% of the isoprenaline maxima. A small positive chronotropy (16.5 +/- 5.6% maximum) of right atria occurred. After pretreatment with reserpine (1.0 mg kg-1 i.p. daily) for 7 days, the three preparations displayed supersensitivity to isoprenaline, revealed as a significant displacement (P less than 0.05) of the concentration-response curves to the left of those for control rats. Reserpine pretreatment, however, had no effect on the sensitivity to methoxamine. The increase in beta-adrenoceptor sensitivity to isoprenaline after reserpine pretreatment was accompanied by a significant 41.3% increase (P less than 0.05) in the number of [3H]-dihydroalprenolol [( 3H]-DHA) binding sites (Bmax) in ventricular membranes, although the dissociation constant (KD) was unaffected. There were more alpha-adrenoceptor [3H]-prazosin binding sites in ventricular than atrial membranes. However, there was no difference in KD or Bmax between reserpine-pretreated and control tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Nicotine antagonizes the effects of reserpine on the striatal metabolism of dopamine, 5-hydroxytryptamine and noradrenaline in hypothermic but not in normothermic mice.

Our previous studies indicate that repeated nicotine administration inhibits the release of striatal dopamine in hypothermic mice. To study if similar inhibition occurs in noradrenergic and serotoninergic neurons mice were given (-)-nicotine (3 mg/kg, s.c.) repeatedly at 110, 80, 50, and 20 min before sacrifice. The interactions of nicotine with reserpine were also investigated. Reserpine (5 mg/kg, i.p.) was administered after the second nicotine dose at 60 min before sacrifice. To prevent the effects of nicotine on autonomic ganglia all mice were given hexamethonium (10 mg/kg, i.p.). Experiments were carried out at 20-22 degrees C at which ambient temperature nicotine induced deep hypothermia or at 32-34 degrees C to prevent the drug-induced hypothermia. The changes in striatal metabolism of dopamine, noradrenaline and 5-hydroxytryptamine (5-HT) we Nicotine had temperature dependent effects on the dopamine metabolism which indicates a block of dopaminergic neurons as suggested in our earlier studies. Reserpine per se increased the homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) contents and decreased the 3-methoxytyramine (3-MT) and dopamine contents at both ambient temperatures. In hypothermic but not in "normothermic", nicotine-treated mice reserpine's effect on dopamine metabolism was almost totally vanished. Nicotine and reserpine per se increased the 3-methoxy-4-hydroxyphenylethylglycol (MOPEG) content and decreased the noradrenaline content at both ambient temperatures. In hypothermic but not in "normothermic" mice nicotine antagonized the reserpine-induced decrease of noradrenaline content. Nicotine tended to decrease the 5-hydroxy-indoleacetic acid (5-HIAA) content in hypothermic mice but increased it in "normothermic" ones.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Alteration of basal ganglia evoked responses by reserpine and L-dopa.

The effects of reserpine and L-Dopa on basal ganglia evoked potentials were investigated in cats. The caudate response resulting from substantia nigra stimulation and the substantia nigra response elicited by globus pallidus stimulation were increased at several hours after the systemic administration of reserpine. L-Dopa in the presence of dopa decarboxylase inhibition (MK-486) depressed these responses and reversed the effect of reserpine at 0.5 h after administration. Reserpine did not reverse the L-Dopa effect. Reserpine and L-Dopa caused no significant change in responses between other basal ganglia structures. These data give evidence that the basal ganglia are major sites for reserpine and L-Dopa action.

Animals↗