Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Reserpine”

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

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

At least 703 records · Page 39Linked to original sources
PubMed2002

The mitochondrial toxin 3-nitropropionic acid aggravates reserpine-induced oral dyskinesia in rats.

The effects of a previous long-term administration of the mitochondrial toxin 3-nitropropionic acid were studied on an animal model of tardive dyskinesia, i.e., the frequency of spontaneous tongue protrusions in rats repeatedly treated with reserpine. 3-Nitropropionic acid (10 or 15 mg/kg i.p., every other day for 17 days) potentiated the increase in tongue-protrusion frequency induced by reserpine (1 mg/kg, s.c., every other day for 3 days) but did not modify reserpine-induced increase in immobility duration and decrease in locomotion frequency. These results support the notion that neurotoxic events are associated with the development of tardive dyskinesia.

Adrenergic Uptake Inhibitors↗
PubMed2000

Dual effects of L-3,4-dihydroxyphenylalanine on aromatic L-amino acid decarboxylase, dopamine release and motor stimulation in the reserpine-treated rat: evidence that behaviour is dopamine independent.

The comparative effects of L-3,4-dihydroxphenylalanine (L-DOPA) on dopamine synthesis, release and behaviour were studied in the reserpine-treated rat. Acute administration of L-DOPA (25-200 mg/kg) dose-dependently inhibited the activity of aromatic L-amino acid decarboxylase (AADC) in the substantia nigra and corpus striatum. The antiparkinsonian drugs budipine (10 mg/kg) and amantadine (40 mg/kg) enhanced AADC activity in these regions, and prevented or reversed AADC inhibition by L-DOPA. Dual probe dialysis revealed that low doses of L-DOPA (25-50 mg/kg) dose-dependently stimulated the release of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in nigra and striatum, whilst high doses of L-DOPA (100-200 mg/kg) completely suppressed the release of dopamine, but not DOPAC. Sulpiride (50 microM) administered via the probes antagonized dopamine release in response to 25 mg/kg L-DOPA, but greatly facilitated release by 200 mg/kg L-DOPA. Dopamine release was blocked by the centrally acting AADC inhibitor NSD 1015, but facilitated by the central AADC activator budipine. In behavioural tests L-DOPA (plus benserazide, 50 mg/kg) only reversed akinesia at 200 mg/kg, and not at 25-100 mg/kg. Pretreatment with either NSD 1015 (100 mg/kg) or budipine (10 mg/kg) markedly potentiated the motor stimulant action of a threshold dose of L-DOPA (100 mg/kg). A combination of NSD 1015 (100 mg/kg) and benserazide (50 mg/kg) potentiated L-DOPA behaviour more effectively than either inhibitor alone. NSD 1015-facilitated L-DOPA behaviour was antagonized by sulpiride (100 mg/kg) and not by SCH 23390 (1 mg/kg), whereas budipine-facilitated L-DOPA behaviour was fully antagonized by SCH 23390 and only partially by sulpiride. These results show that behaviourally active doses of L-DOPA in the reserpinized rat are not accompanied by significant increases in extracellular dopamine and are therefore probably not dopamine mediated. We propose that L-DOPA is capable of directly stimulating dopamine D2 and possibly non-dopamine receptors, thereby inhibiting dopamine efflux presynaptically and promoting motor activation postsynaptically. A stimulant action of L-DOPA on motor behaviour, preferentially mediated by D1 > D2 receptors, suggests that L-DOPA may also be capable of yielding a dopamine-like response in the absence of detectable dopamine release. These findings are incorporated into a new model of L-DOPA's actions in the reserpinized rat, and their possible implications for our understanding of L-DOPA in Parkinson's disease are discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Reserpine effects on neurotransmitters in chick heart during growth.

Effects of tranquilizing agents on neurotransmitters in the heart have not been widely studied. Thus, the effect of intraperitoneal injection of reserpine, (2.5 mg/kg bw) on the concentrations of excitatory (glutamic acid, glutamine, aspartic acid, asparagine), inhibitory (GABA, glycine, alanine, taurine), neurotransmitters as well as the enzymes (GOT and GPT) and total protein were measured in both heart and serum chicks at different ages (1, 7, 30, 90 and 180 days). Reserpine induced a decrease in the excitatory amino acids and an increase in GABA in both heart and serum in most ages. Glycine and alanine increased in the heart and decreased in serum. Taurine increased in the heart of young ages (1 and 7 days) and decreased in older ones (90 and 180 days), however, it decreased in serum of most ages. Both GOT and GPT increased in heart but, in serum, GOT increased and GPT decreased in most ages. Total protein increased in the heart of young chicks and decreased in the 90- and 180-day-old chicks. In conclusion, reserpine induced a parallel decrease in the ratio glutamate, glutamine, aspartate/GABA in both myocardial tissue and serum of the different age groups. Changes observed in neurotransmitters of the heart suggest that these amino acids may play a similar role in the myocardial tissue, as is described in the central nervous system.

Aging↗
PubMed1988

Beneficial effects of intra-arterial reserpine after upper-extremity embolectomy: a prospective randomised trial.

Persistent ischaemia occasionally follows technically-successful arterial embolectomy, and has generally been ascribed to small-vessel thrombosis in the distal vascular bed. Because of the possibility that distal vasospasm might be a contributory cause, we conducted a prospective randomised trial of vasodilator therapy in this setting. In 50 consecutive patients presenting with their first episode of upper-extremity arterial embolism, we compared the results of the intra-arterial instillation of 0.5 mg reserpine with those of saline alone following embolectomy. Among 29 patients receiving saline only, 13 (44.8%) suffered persistent or recurrent limb ischaemia requiring reoperation, while three (14.3%) of 21 patients receiving reserpine had continuing ischaemia (P = 0.02). Three patients in each group required a second re-operation; all three in the reserpine group were ultimately found to have a proximal axillo-subclavian artery stenosis as the cause for their persistent or recurrent limb ischaemia. Although its underlying pathophysiology remains obscure, peripheral vasospasm appears to accompany acute embolic arterial occlusion. Manoeuvres to prevent or reverse such distal vasoconstriction may be useful in avoiding persistent or recurrent ischaemia following arterial embolectomy.

Aged↗
PubMedDate not supplied

Concentrations of biogenic amines in fundal layers in chickens with normal visual experience, deprivation, and after reserpine application.

Previous experiments in chickens have shown that dopamine released from the retina may be one of the messengers controlling the growth of the underlying sclera. It is also possible, however, that the apparent relationship between dopamine and myopia is secondary and artifactual. We have done experiments to assess this hypothesis. Using High Pressure Liquid Chromatography with electrochemical detection (HPLC-ED), we have asked whether changes in dopamine metabolism are restricted to the local retinal regions in which myopia was locally induced. Furthermore, we have measured the concentrations of biogenic amines separately in different fundal layers (vitreous, retina, choroid, and sclera) to find out how changes induced by "deprivation" (= removal of high spatial frequencies from the retinal image by translucent eye occluders which produce "deprivation myopia") are transmitted through these layers. Finally, we have repeated the deprivation experiments after intravitreal application of the irreversible dopamine re-uptake blocker reserpine to see how suppression of dopaminergic transmission affects these changes. We found that (1) Alterations in retinal dopamine metabolism were indeed restricted to the retinal areas in which myopia was induced. (2) The retina was the major source of dopamine release with a steep gradient both to the vitreal and choroidal side. Vitreal content was about one-tenth, choroidal content about one-third, and scleral content about one-twentieth of that of the retina. (3) There was a drop by about 40% in vitreal dopamine, DOPAC (3,4-dihydroxyphenylacetic acid) and HVA (homovanilic acid) concentrations following deprivation which occurred already at a time where little changes could yet be seen in their total retinal contents. (4) Choroidal and scleral dopamine levels were not affected by deprivation, indicating that other messengers must relay the information to the sclera. (5) A single intravitreal injection of reserpine lowered dopamine and HVA levels in retina and vitreous for at least 10 days in a dose-dependent fashion and diminished or suppressed further effects of deprivation on these compounds. DOPAC levels continued to change upon deprivation even after reserpine injection (Fig. 3). Our results suggest that the release rates of dopamine from retinal amacrine cells can be estimated from vitreal dopamine concentrations; furthermore, they are in line with the hypothesis that there is an inverse relationship between dopamine release and axial eye growth rates. Although our experiments do not ultimately prove that dopamine has a functional role in the visual control of eye growth, they are in line with this notion.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

The 5HT(1B) receptor agonist, CP-93129, inhibits [(3)H]-GABA release from rat globus pallidus slices and reverses akinesia following intrapallidal injection in the reserpine-treated rat.

This study examined whether activation of 5HT(1B) receptors in the rodent globus pallidus (GP) could reduce GABA release in vitro and reverse reserpine-induced akinesia in vivo. Microdissected slices of GP from male Sprague Dawley rats (300-350 g) were preloaded with [(3)H]-GABA. During subsequent superfusion, 4 min fractions were collected for analysis of release. The effects of the 5HT(1B) receptor agonist, 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3, 2-b]pyrid-5-one (CP-93129), on 25 mM KCl-evoked release were examined using a standard dual stimulation paradigm. Male Sprague Dawley rats (270 - 290 g), stereotaxically cannulated above the GP, were rendered akinetic by injection of reserpine (5 mg kg(-1) s.c.). Eighteen hours later, the rotational behaviour induced by unilateral injection of CP-93129 was examined. CP-93129 (0.6-16.2 microM) produced a concentration-dependent inhibition of 25 mM KCl-evoked [(3)H]-GABA release reaching a maximum inhibition of 52.5+/-4.5%. The effect of a submaximal concentration of CP-93129 (5.4 microM) was fully inhibited by the 5HT(1B) receptor antagonist, isamoltane (10 microM). Following intrapallidal injection, CP-93129 (30-330 nmol in 0.5 microl) produced a dose-dependent increase in net contraversive rotations reaching a maximum of 197+/-32 rotations in 240 min at 330 nmol. Pre-treatment with isamoltane (10 nmol in 1 microl) inhibited the effects of a submaximal dose of CP-93129 (220 nmol) by 84+/-6%. These data suggest that at least some 5HT(1B) receptor function as heteroreceptors in the GP, reducing the release of GABA. Moreover, CP-93129-mediated activation of these receptors in the GP provides relief of akinesia in the reserpine-treated rat model of PD.

Animals↗
PubMed2003

GABA(B) receptor agonists reverse akinesia following intranigral or intracerebroventricular injection in the reserpine-treated rat.

1. This study examined whether GABA(B) receptor agonists injected directly into the substantia nigra pars reticulata (SNr) and globus pallidus (GP), or given intracerebroventricularly, could reverse reserpine-induced akinesia in the rat. 2. Male Sprague-Dawley rats, stereotaxically cannulated above the SNr, GP or third ventricle, were rendered akinetic by injection of reserpine (5 mg kg(-1) s.c.). After 18 h, the locomotor effects of the GABA(B) receptor agonists, baclofen or SKF 97541 were examined. 3. Unilateral injection of baclofen (1-5 micro g in 0.5 micro l) into the GP failed to evoke any locomotor response (n=6). In contrast, unilateral intranigral injection of baclofen (0.08-1.6 micro g in 0.5 micro l) produced a dose-dependent increase in net contraversive rotations reaching a maximum of 162+/-24 turns 90 min(-1) (n=6-8). Pretreatment with the selective GABA(B) receptor antagonist, CGP 46381 (2.4 micro g in 0.5 micro l), inhibited the effects of baclofen (0.8 micro g) by 68+/-9% (n=6). 4. Following intracerebroventricular injection, baclofen (0.8-4 micro g in 2 micro l) produced a dose-dependent increase in net arbitrary locomotor units (ALUs), reaching a maximum of 447+/-154 ALUs in 35 min (n=6-7). SKF 97541 (4-32 micro g in 2 micro l) similarly reversed akinesia, reaching 129+/-69 ALUs in 15 min (n=6). 5. These data show that activation of GABA(B) receptors within the SNr, but not the GP, reverses reserpine-induced akinesia. The success of intracerebroventricular injection of baclofen suggests a potential for systemically active GABA(B) receptor agonists in the treatment of akinesia in Parkinson's disease.

Animals↗
PubMed2000

Chemiluminometric determination of reserpine and related alkaloids.

The determination of the alkaloids reserpine, rescinnamine and yohimbine based on a chemiluminogenic reaction with potassium permanganate in the presence of polyphosphoric acid is described. The investigation was carried out using a batch and a flow injection chemiluminometer. Both approaches were accurate and precise, allowing the measurement of reserpine within the ranges 0.100-3.00 and 0.050-3.00 micrograms ml-1 with RSD values for 1.00 microgram ml-1 of 1.91 and 0.33% (n = 8) with the batch and the flow injection manifold, respectively. The procedure was successfully applied to formulations after extraction of reserpine with chloroform, with recoveries from commercial formulations within the range 95.2-99.0%.

Adrenergic alpha-Antagonists↗
PubMed1976

Relative effectiveness of chlorothiazide, reserpine and hydrallazine in spontaneously hypertensive rats.

1. Previous studies in this laboratory indicated that a mixture of anti-hypertensive agents in the drinking water controlled the blood pressure of spontaneously hypertensive rats (SHR). The present study was designed to determine which of the agents exerted the greatest anti-hypertensive effect. 2. Treatment was begun at 12 weeks of age in groups of eleven to seventeen rats with one of the following drugs: reserpine, chlorothiazide or hydrallazine. Blood pressures were recorded by the tail method under light ether anaesthesia every 2 weeks until the rats were approximately 70 weeks of age. 3. At 50 weeks of age, blood pressure of chlorothiazaide-treated rats averaged 40 mmHg below untreated control SHR; reserpine-treated SHR were also 40 mmHg lower than control rats, and hydrallazine-treated SHR were 85 mmHg below the control rats. 4. Rats in all groups gained weight normally and appeared in good health. Although all drugs were active, hydrallazine was considerably more effective than chlorothiazide or reserpine in the SHR.

Animals↗
PubMed1999

Acute reserpine treatment alters the catecholamine, glucocorticoid and opioid response to walking exercise in sheep.

The aim of the study was to examine the effects of reserpine on the plasma levels of adrenaline, noradrenaline, cortisol and alpha-neoendorphin in sheep under control conditions and during walking exercise. One hour of walking (5 km/h) caused a significant increase in both catecholamines and cortisol between 10 and 30 min of stress, and transiently decreased the level of alpha-neoendorphin at the same time. Reserpine at the dose of 0.3 mg/kg i.v. given before stress significantly lowered the basal levels of all tested parameters. A combination of the reserpine and walking exercise significantly attenuated the stress-induced changes in the plasma level of measured hormones.

Adrenergic Uptake Inhibitors↗
PubMed2003

The myth of reserpine-induced depression: role in the historical development of the monoamine hypothesis.

For five decades it has been generally accepted that reserpine, an antihypertensive and antipsychotic drug, causes depression. The discovery that reserpine depletes brain monoamines was an important factor in the development of the monoamine hypothesis of depression, and it continues to be widely cited in support of this hypothesis. The present paper argues that, contrary to prevailing belief, reserpine is not depressogenic. The reason for perpetuation of this myth is reluctance to discard the monoamine hypothesis. This hypothesis ushered the modern biochemical paradigm into psychiatry and is still of great importance. It serves as a heuristic to guide research, it enhances psychiatry's prestige, and it helps to validate and promote drug therapy for depression and other mental disorders.

Biogenic Monoamines↗
PubMed1978

Short-term stressor effects of reserpine.

The effects of reserpine on plasma glucose, FFA and cholesterol and on adrenal cholesterol were determined in 1-and 21-d-old chicks over a 24-h period. 2. Irrespective of age, reserpinised chicks became hyperglycaemic and hypocholesteraemic, their stores of adrenal cholesterol were depleted and the mobilisation of the lipid was impaired. The response of the older bird was quantitatively larger than that of the younger bird. 3. Propranolol prevented the increase in plasma glucose concentration seen 1 h after reserpine but it did not affect subsequent changes. 4. It is concluded that reserpine acts as a stressor and it is shown that its effects have not been entirely overcome after 24 h.

Adrenal Glands↗
PubMedDate not supplied

Evaluation of the Xpa-deficient transgenic mouse model for short-term carcinogenicity testing: 9-month studies with haloperidol, reserpine, phenacetin, and D-mannitol.

As part of the international evaluation program coordinated by ILSI/HESI, the potential of DNA repair deficient Xpa-/- mice and the double knockout Xpa-/-.p53+/- mice for short term carcinogenicity assays was evaluated. For comparison also wild-type C57BL/6 mice (WT) were included in these studies. Four test compounds were administered to groups of 15 male and 15 female Xpa-/- mice, Xpa-/-.p53+/- mice and WT mice for 39 weeks. The model compounds investigated were haloperidol, reserpine (nongenotoxic rodent carcinogens, putative human noncarcinogens), phenacetin (genotoxic rodent carcinogen, suspected human carcinogen), and D-mannitol (noncarcinogen in rodents and humans). The test compounds were administered as admixture to rodent diet at levels up to 25 mg/kg diet for haloperidol, 7.5 mg/kg diet for reserpine, 0.75% for phenacetin, and 10% for D-mannitol. These levels included the maximum tolerable dose (MTD). Survival was not affected with any of the test compounds. Haloperidol, reserpine and D-mannitol were negative in the carcinogenicity assay with Xpa-/- and Xpa-/-.p53+/- mice, showing low and comparable tumor incidences in controls and high-dose animals. The results obtained with phenacetin may be designated equivocal in Xpa-/-.p53+/- mice, based on the occurrence of a single rare tumor in the target organ (kidney) accompanied by a low incidence of hyperplastic renal lesions and a high incidence of karyomegaly. These results are in agreement with the currently known carcinogenic potential of the 4 test compounds in humans.

Administration, Oral↗
PubMed1983

Mechanism of uptake and retrograde axonal transport of noradrenaline in sympathetic neurons in culture: reserpine-resistant large dense-core vesicles as transport vehicles.

The uptake and retrograde transport of noradrenaline (NA) within the axons of sympathetic neurons was investigated in an in vitro system. Dissociated neurons from the sympathetic ganglia of newborn rats were cultured for 3-6 wk in the absence of non-neuronal cells in a culture dish divided into three chambers. These allowed separate access to the axonal networks and to their cell bodies of origin. [3H]NA (0.5 X 10(-6) M), added to the axon chambers, was taken up by the desmethylimipramine- and cocaine-sensitive neuronal amine uptake mechanisms, and a substantial part was rapidly transported retrogradely along the axons to the nerve cell bodies. This transport was blocked by vinblastine or colchicine. In contrast with the storage of [3H]NA in the axonal varicosities, which was totally prevented by reserpine (a drug that selectively inactivates the uptake of NA into adrenergic storage vesicles), the retrograde transport of [3H]NA was only slightly diminished by reserpine pretreatment. Electron microscopic localization of the NA analogue 5-hydroxydopamine (5-OHDA) indicated that mainly large dense-core vesicles (700-1,200-A diam) are the transport compartment involved. Whereas the majority of small and large vesicles lost their amine dense-core and were resistant to this drug. It, therefore, seems that these vesicles maintained the amine uptake and storage mechanisms characteristic for adrenergic vesicles, but have lost the sensitivity of their amine carrier for reserpine. The retrograde transport of NA and 5-OHDA probably reflects the return of used synaptic vesicle membrane to the cell body in a form that is distinct from the membranous cisternae and prelysosomal structures involved in the retrograde axonal transport of extracellular tracers.

Animals↗
PubMed2006

Quantitative determination of reserpine, ajmaline, and ajmalicine in Rauvolfia serpentina by reversed-phase high-performance liquid chromatography.

A sensitive and reproducible reversed-phase high-performance liquid chromatography (HPLC) method using photodiode array detection is established for the simultaneous quantitation of important root alkaloids of Rauvolfia serpentina, namely, reserpine, ajmaline, and ajmalicine. A Chromolith Performance RP-18e column (100 x 4.6-mm i.d.) and a binary gradient mobile phase composed of 0.01 M (pH 3.5) phosphate buffer (NaH(2)PO(4)) containing 0.5% glacial acetic acid and acetonitrile are used. Analysis is run at a flow rate of 1.0 mL/min with the detector operated at a wavelength of 254 nm. The calibration curves are linear over a concentration range of 1-20 microg/mL (r = 1.000) for all the alkaloids. The various other aspects of analysis (i.e., peak purity, similarity, recovery, and repeatability) are also validated. For the three components, the recoveries are found to be 98.27%, 97.03%, and 98.38%, respectively. The limits of detection are 6, 4, and 8 microg/mL for ajmaline, ajmalicine, and reserpine, respectively, and the limits of quantitation are 19, 12, and 23 microg/mL for ajmaline, ajmalicine, and reserpine, respectively. The developed method is simple, reproducible, and easy to operate. It is useful for the evaluation of R. serpentina.

Ajmaline↗
PubMed1989

The effect of reserpine and guanethidine on carbohydrate metabolism in ischaemic rat myocardium.

We have investigated the role of endogenous catecholamines in myocardial carbohydrate metabolism in isolated, perfused rat hearts after left coronary artery occlusion for 30 min. A significant decrease in ATP and glycogen, and an increase in glucose-6-phosphate (G-6-P) content in the ischaemic myocardium was obtained. After depletion of the cardiac noradrenaline stores by reserpine or guanethidine pretreatment the increase in the G-6-P levels was very markedly enhanced, and the myocardial glycogen content of non-ischaemic control hearts was significantly increased by reserpine. However, the amount of glycogen broken down during the ischaemia in pretreated animals was similar to that in the ischaemic myocardium from control animals, and the decrease in the myocardial ATP was not altered by reserpine or guanethidine. Thus the well known release of noradrenaline during myocardial ischaemia is not an essential prerequisite for the activation of the ischaemic breakdown of glycogen. Rather, it is of importance for later steps in anaerobic carbohydrate metabolism, probably for the activation of phosphofructokinase, as suggested by the large ischaemic accumulation of G-6-P in noradrenaline depleted hearts.

Adenosine Triphosphate↗
PubMed1981

PGO wave activity and cortical EEG in the reserpinized, anesthetized cat.

We have studied ponto-geniculo-occipital (PGO) spike rhythms and the relation of PGO spikes to degrees of cortical electroencephalographic (EEG) synchrony in the reserpinized, anesthetized cat. Even under reserpine, PGO waves occur with a definite rhythmic character having a basic rhythm of approximately 30-35 min, which is similar to the normal sleep EEG cycle in cats. After peaking in each cycle, PGO activity rates either dropped to zero or fell to very low values. Cortical EEG activity, particularly in the frontal cortex, was clearly related to the density of PGO waves. In periods of dense PGO waves the frontal cortex was most synchronized and the degree of synchrony diminished as the PGO wave rate fell. In most instances during periods of EEG desynchronization, no PGO waves were present. Coherence values between frontal and occipital cortices were greatest during high PGO spike activity. These studies show that even under reserpine, a basic PGO rhythmicity is maintained and that in this preparation there is a clear association of high PGO wave density and cortical EEG synchronization.

Anesthesia, General↗