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At least 19 recordsLinked to original sources
PubMed1977

[Effects of reserpine and its derivatives on release of biogenic amines. Comparative study of the activity of reserpine and diethylaminoethyl-1-reserpine as bitartrates (author's transl)].

A comparative study of the activity of reserpine and its salt of diethylamineothyl on the central nervous system was performed. Palpebral ptosis in the mouse and depletion of catecholamines in the rat served for comparison. The reserpine salt of diethylaminoethane is a new derivative of reserpine the depleting activity of which on the central nervous system is considerably diminished.

Animals↗
PubMed1979

Antibody specificity studies for reserpine, its metabolites, and synthetic reserpine congeners: radioimmunoassay.

Progress in the development of radioimmunoassay techniques for reserpine and related compounds is reported. A conjugate of reserpine with human serum albumin was prepared, involving linkage at the indole nitrogen atom of reserpine. Injection of the purified conjugate into sheep elicited antibodies of high titer, which bound reserpine selectively. Tritiated reserpine was employed in the procedure, and dextran-coated charcoal was utilized to separate free and bound forms of the drug. Antibodies exhibited a selectivity for reserpine and did not cross-react significantly with major human metabolites. Cross-reactivity of antibodies with other reserpine derivatives (i.e., syrosingopine, deserpidine, and rescinnamine) also was investigated. A stable tritiated or radioiodinated reserpine derivative of high specific activity is being sought to improve assay sensitivity for use in bioequivalence and bioavailability studies. In the absence of any extraction or concentration procedures, at least a 10-fold increase in immunoassay sensitivity would be required to follow reserpine levels in humans given normal doses of the drug. The methods show promise also for the assay of reserpine derivatives such as deserpidine, which exhibits cross-reactivity to reserpine antibodies.

Animals↗
PubMed1976

The biological fate of reserpine.

Orally administered reserpine is readily absorbed from the GI tract. During this process at least a portion of the drug is metabolized by the intestinal mucosa and then presumably is acted upon by serum esterases. Methylreserpate and trimethoxybenzoic acid are the primary metabolites which result from the hydrolytic cleavage of reserpine. Since most of the blood leaving the GI tract passes through the liver via the portal vein, hepatic metabolism would also be expected to reduce reserpine levels in the blood. The relative contributions of serum esterases versus hepatic metabolism in the biotransformation of reserpine in vivo are not known. However, very little unmetabolized reserpine is eventually eliminated in the urine. In the liver, it is quite likely that both microsomal oxidative and hydrolytic enzymes contribute to the metabolism of reserpine. It seems that microsomal oxidation (such as the demethylation of the 4-methoxy group on the TMBA moiety) must precede hydrolysis since inhibition of demethylation markedly reduces the rate of hydrolysis. In addition to oxidation and hydrolysis, conjugative reactions also must occur in liver or extrahepatic tissues since both glucuronide and sulfate conjugates of TMBA have been identified. Some reserpine molecules do seem to escape metabolism, however, since significant amounts of intact reserpine have been found in fecal samples taken from both experimental animals and human beings after either oral or parenteral drug administration. Presumably reserpine is transported from the blood via the biliary tree into the small intestine where it is either reabsorbed or eliminated in the feces. Pulmonary elimination of CO2 produced after complete oxidation of the 4-methoxy group of TMBA has also been shown to occur both in vivo and in vitro. The following may serve as a model for the relationship between the subcellular distribution of reserpine and its site of action. After a single intravenous injection most of the reserpine, probably loosely bound to plasma albumin, is distributed to tissues on the basis of their blood flow. Because of its lipophilic properties, reserpine would easily penetrate cell membranes and then bind possibly electrostatically to intracellular membrane components, particularly those rich in phospholipids. Much of the circulating reserpine would then either be metabolized or be taken up by the lipid depots of the body, leading to a rapid redistribution of the reversibly bound reserpine from the tissues. During this time a relatively small fraction of the total reserpine administered by injection would become associated with monoaminergic granular membranes in a more specific and irreversible manner. This would result in a persistent, nonstoichiometric inhibition of monoamine uptake. Such a small specific binding would not be detectable for at least 18 hr after reserpine administration, i.e., until most of the reversibly bound alkaloid had been metabolized and/or excreted...

Animals↗
PubMed1976

[The action of reserpine on the concentration of 5-hydroxytryptamine, epinephrine and norepinephrine in the venous blood of migraine patients].

Vasoactive amines, particularly 5-hydroxy-tryptamine (5-HT) have been implicated as the cause of migraine. Our study was a biochemical one on the effect of reserpine on the content of 5-HT, NE and E in migraneurs. The effect of one single infection of reserpine. 23 migrainous patients and 7 controls were given one i.m. injection of reserpine (1,5 mg/1.7 m2 surface). The content of 5-HT in blood platelets of 8 migraneurs and 7 controls 6 hours after the injection of reserpine decreased to comparable levels in both groups. The serotonin releasing effect of reserpine, however, is different from that of tyramine. The effect of prolonged reserpine medication. The effect of i.v. injection of reserpine over a period of 6 weeks on 5-HT, NE and E, was investigated. The doses of reserpine corresponded exactly to the doses already used by Nattero et al. (0.2 mg reserpine 3 times a week for 6 weeks). In correspondance with this work a double blind clinical examination was carried out by Nattero et al. (1975). Blood amine levels were measured weekly. The NE decreased to a minimum of 62% of basal mean value after 3-7 weeks of treatment. The decrease is significant from the third to the sixth week. Basal value was not reached until 6 weeks after withdrawal of reserpine. The concentration of 5-HT in blood platelets decreased to 5% of basal mean value and remained low during the reserpine treatment. The decrease is highly significant. A clinical improvement began 1-2 weeks after the introduction of reserpine treatment, continued during treatment and for 2-6 weeks after. In the open trial performed by us, we can confirm the results of Nattero et al. We demonstrated a marked decrease in concentration of blood amines corresponding to clinical improvement.

Epinephrine↗
PubMed1975

On the formation of adrenergic amine storage granules as measured by reserpine labeling.

Reserpine appears to be bound specifically and irreversibly to amine storage granules in the adrenergic neuron. The presence of reserpine persistently attached to amine granule should reflect the life span of the vesicles, and any additional binding of reserpine should then measure the rate of appearance of newly formed amine granules. Measurement of the persistent binding of tritiated reserpine (3H-Reserpine) in hearts of rats given labeled compound at various times after a saturating dose of unlabeled reserpine showed that the recovery of 3H-reserpine binding capacity occurred rapidly. Four days after reserpine the 3H-reserpine binding was 30% of control rats. The rate of return of binding capacity was then slowed being 65% of normal in 24 days. Calculation of the mean daily increment of binding capacity showed that the rate was an inverse linear function of the binding capacitu existing in the neurone at an early phase (1--8 days) but became constant at a later interval (8--24 days). It is suggested that the return of reserpine binding capacity reflects the appearance of new storage granules and that the rate of storage granule synthesis in the cell body is under feedback control. The signal for enhanced granule formation does not appear to be related to the intensity of nerve traffic not to the concentration of transmitter in the neuron since manaeuvers which alter these parameters did not change the rate of reserpine binding recovery.

Amines↗
PubMed1979

Reduction by reserpine of the accumulation of retrogradely transported [125I]nerve growth factor in sympathetic neurons.

Experiments were carried out to determine if stimuli which augment preganglionic nerve activity to sympathetic neurons, and thereby cause trans-synaptic induction, increase the retrograde transport of nerve growth factor (NGF). It was found that nerve activity had no effect on retrograde transport of [125I]NGF. It was found, however, that reserpine decreased retrograde transport of [125I]NGF and this inhibition was characterized. Reserpine decreased the maximal accumulation of intravenously administered [125I]NGF in superior cervical ganglia (SCG) by about 60%. It also caused a distinct shift in the time course of accumulation so that maximal accumulation was seen 12 h after [125I]NGF injection rather than at 9 h as in control animals. Reserpine had no effect on retrograde transport in sensory neurons. Dose--response curves showed that maximal inhibition occurred with doses of reserpine of 2.5 mg/kg i.p. and that reserpine was not able to completely block transport at any dose. The maximal inhibition of retrograde transport was achieved within 30 min of reserpine administration and inhibitory activity was unchanged for 36 h. The ability of sympathetic neurons to transport [125I]NGF subsequently recovered and was normal 96 h after reserpine administration. The inhibitory effect of reserpine appears to be due to an action at or very near to the nerve terminal since it was effective at reducing NGF transport at very low doses (0.33 microgram) when co-administered directly into the eye with [125I]NGF. An action of reserpine at the nerve terminal was further suggested by the inability of reserpine to affect transport if the drug was given 4 h after [125I]NGF administration. Based upon these data, it is suggested that there may be two pools of retrogradely transported NGF and that only more rapidly turning over pool is reserpine-sensitive. This pool may represent the retrogradely moving synaptic vesicles or some derivative of the vesicles.

Animals↗
PubMed1991

Alterations of amylase secretion in the chronically reserpinized rat: an acetylcholine-mediated phenomenon.

Chronic reserpine treatment of animals, an experimental model for cystic fibrosis (CF), results in generalized exocrinopathy, impaired secretion, and decreased pancreatic content of amylase. However, the mechanisms of altered acinar pancreatic function in both CF patients and reserpine-treated rats are still unknown. The present study was designed to investigate the secretory response of the rat pancreas after reserpine treatment. Rats were given reserpine (1 mg kg-1 day-1 ip) or vehicle, and killed 2, 4, or 7 days later. To distinguish between specific effects of reserpine and those related to secondary malnutrition caused by the drug, secretory response of a group of pair-fed animals to reserpine was also investigated. During reserpine treatment, body weight and food intake were significantly reduced from the 2nd day on. Amylase release from dispersed pancreatic acini, prepared from control pair-fed and from reserpine-treated rats were used to evaluate functional secretory capacity. After 7 days, both chronic reserpine and pair-feeding significantly decreased pancreatic amylase concentration to 75 and 50% of controls, respectively. Reserpine caused desensitization of the pancreatic acini secretory response to carbamylcholine, without altering maximal amylase release. Desensitization occurred gradually and reached a maximum after 7 days. Secretory responses to caerulein and to the phorbol ester 12.0-tetradecanoyl phorbol-13 acetate (TPA) were not altered. These findings indicate that desensitization of amylase release after reserpine was specific to this muscarinic agonist. It may result from increased endogenous acetylcholine release in the course of treatment.

Acetylcholine↗
PubMed1976

[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives].

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.

Acetates↗
PubMed1991

Transsynaptic activity regulates proenkephalin and tyrosine hydroxylase gene expression and the response to reserpine in the hamster adrenal.

Transsynaptic neurogenic activity and reserpine are two signals that cause the proenkephalin (Penk) gene to alter the levels of preproenkephalin (PPenk) mRNA and enkephalin-containing (EC) peptides. In the Syrian hamster adrenal, but not in rat adrenal, both of these signals appear to be positive activators of Penk gene expression. The separate and combined effects of reserpine and denervation on EC peptides and catecholamine systems were investigated in the adrenal of the hamster, a species with relatively high medullary PPenk mRNA and EC peptide levels. Unilateral adrenal denervation resulted in a rapid decrease in PPenk mRNA levels of 54% after 2 days, and by 11 days 90% of Penk mRNA had disappeared. After 4 days both EC peptide and PPenk mRNA levels fell in parallel, whereas total RNA and soluble protein levels were unchanged. Denervation had no effect on TH mRNA levels until 8 days after surgery, and after 11 days both TH mRNA and catecholamine levels had decreased by 35-45%. Reserpine produced a dose- and time-dependent depletion of EC peptides and catecholamines. One day after 5 mg/kg reserpine (given subcutaneously on each of 2 consecutive days), EC peptides were reduced by 80%, norepinephrine by 79%, and epinphrine by greater than 95%. By 4 days after treatment, EC peptides and catecholamines slightly exceeded or had returned to control (concurrent vehicle treatment) values. PPenk mRNA levels, as measured by solution hybridization, were doubled (206 +/- 17%, mean +/- standard error) by day 4. Tyrosine hydroxylase (TH) mRNA levels were increased nearly 7-fold (686 +/- 71%) 24 hr after the first reserpine dose and declined thereafter. Northern blot analysis demonstrated that reserpine did not alter the size of either PPenk or TH mRNAs. Size exclusion chromatography showed a small (20%) reserpine-induced increase in processing of high molecular weight Penk-like peptides. The effects of reserpine, which increases PPenk mRNA, EC peptides, and TH mRNA, were completely blocked by unilateral denervation, whereas the contralateral innervated gland showed the expected responses. The co-localized EC peptide and catecholamine systems, as reflected in their mRNAs, respond differently in both time sequence and magnitude to reserpine and to denervation. Our results support a critical role, in vivo, for transsynaptic mechanisms in the maintenance of the high levels of Penk gene expression in this species and for the positive activation (mediated by reflex neurogenic stimulation) of reserpine on Penk and TH gene expression.

Adrenal Glands↗
PubMed1975

Loss of body weight as a predictor of reserpine-induced amine depletion.

Loss of body weight was proved to be a convenient and reliable way to predict the degree of reserpine-induced amine depletion after i.p. injections of reserpine (2.5, 5 and 10 mg/kg) and it thus helps reduce variability. Two populations of animals were sharply distinguished lying on either side of the 5% cutoff point within the first 24 hr. One group (approximately 20% of all animals) lost less than 5% of their body weight, showed absence of physiological and behavioural effects, a moderate 5-HT depletion and a moderate 5-HIAA increase. These animals were called 'partially reserpinized'. Another group always lost 5% or more of body weight, exhibited the reserpine syndrome as well as a larger extent of 5-HT depletion and 5-HIAA increase. This group comprised 'reserpinized' rats. There were significant correlations between the percent weight loss and the degree of 5-HT depletion and 5-HIAA increase in the group of 'partially reserpinized' animals. The two groups differed also in the time course of amine changes. Dose had no effect in the differentiation of the two groups but did affect the extent of amine depletion. When reserpine was given i.v. or s.c., all animals were 'reserpinized'. The phenomenon of partial reserpinization is discussed.

Animals↗
PubMed1976

In vitro alteration of the subcellular distribution of 3H-reserpine in the rat forebrain by delta 9-tetrahydrocannabinol.

delta 9-Tetrahydrocannabinol (delta 9-THC) has been reported to attenuate both reserpine-induced serotonin depletion and reserpine-induced hypothermia. We have observed that delta 9-THC preincubation led to a dose-responsive increase in the amount of 3H-reserpine bound to a crude mitochondrial fraction of rat forebrain. The experiments reported here further characterize this phenomenon. Preincubation with delta 9-THC produced a shift in the localization of 3H-reserpine from the incubation medium and the microsomal supernatant (decrease of 66%) to the crude mitochondrial (CM) pellet (increase of 154%). The CM pellet was subfractionated both by differential centrifugation after osmotic shock and by layering on a five-step discontinuous sucrose gradient and centrifuging at 80,000 x g. Osmotic shock with 0.032 M sucrose and centrifugation revealed that the delta 9-THC-induced increase in 3H-reserpine was contained in both the synaptic vesicle fraction (247%) and the fraction containing myelin, ruptured synaptosomes and mitochondria (324%). Separating the CM fraction into five component parts showed that delta 9-THC increased the 3H-reserpine bound by about 275% in the three fractions containing myelin, membrane fragments or mitochondria. Even more dramatic increases (greater than 1000%) were observed in the two fractions containing cholinergic and non-cholinergic nerve endings. In addition, we have determined that many other drugs which are believed to have membrane mediated mechanisms have no effect on the amount of 3H-reserpine bound to the crude mitochondrial fraction. Although other possibilities exist, these data support the hypothesis that delta 9-THC retards the action of reserpine by altering the normal distribution of reserpine in various membrane components of the rat brain.

Animals↗
PubMedDate not supplied

The effect of drugs interfering with biogenic amines metabolism on gastric secretion and reserpine-ulcers development in rats.

The effect of drugs interfering with endogenous catecholamines metabolism on gastric secretion and gastric ulcers development 4 hr following reserpine administration was investigated in rats with chronic gastric fistulas. Drugs inhibiting catecholamine synthesis: alpha-methyl-p-tyrosine (alpha-MT) and sodium diethyldithiocarbamate (DDC) decreased substantially the reserpine-induced gastric acid and pepsin secretion, but only alpha-MT diminished the development of gastric ulcers. Pretreatment with nialamide (NLD) elicited in reserpinized rats a marked inhibition both of gastric secretion and of gastric ulcers development. Dopamine (DA), noradrenaline (NA) and adrenaline (A) decreased the secretion of hydrochloric acid but did not change the intensity of gastric ulcers caused by reserpine. Desipramine strongly inhibited reserpine-induced gastric acid secretion. Reserpine depleted DA, NA and 5-HT stores in the brain and decreased DA and 5-HT levels in the wall of the stomach in which the NA levels were increased. The changes in biogenic amines content induced by drugs in reserpinized rats did not correlate with their influence on gastric secretion and on the development of mucosal ulcers. The inhibitory effect of all of the drugs examined on gastric acid and pepsin secretion in reserpinized rats was accompanied by the inhibition of gastric ulcers formation following NLD and alpha-MT administration only, indicating that ulcer generation following reserpine depends more on changes in mucosal barrier resistance than on gastric acid secretion.

Animals↗
PubMed1976

[Effects of diuretics after pretreatment with reserpine and 6-OH-dopamine (author's transl)].

Experiments were performed on groups of 10 rats each with respect to the influence of systemic denervation by 6-OH-dopamine or reserpine on the diuretic effect of furosemide (3 mg/kg). In order to get a measure for the effectiveness of denervation, the tissue content of norepinephrine in kidneys, submaxillary glands, and hearts was determined by fluorimetric analysis. Neurotransmitter content: Chemical sympathectomy with 6-OH-dopamine resulted in a decrease of tissue norepinephrine down to 25% of the initial value in the kidneys, and down to 29 and 17% in submaxillary glands and hearts, respectively. After reserpine pretreatment the kidney norepinephrine was found decreased down to 28% of the initial concentration. Plasma electrolytes: Pretreatment with 6-OH-dopamine increased the plasma magnesium concentration considerably. Further administration of 3 mg/kg of furosemide had no additional effect. Plasma sodium, however, was significantly decreased, whereas potassium and calcium concentrations remained unchanged. After reserpine administration plasma calcium was found decreased. The effect was additionally enhanced by furosemide. Plasma sodium was found decreased, too, after furosemide, whereas potassium and magnesium remained unchanged after both reserpine and furosemide treatment. Fluid and electrolyte excretion: The diuretic effect of furosemide was not significantly influenced by both 6-OH-dopamine and reserpine pretreatment. In the reserpine pretreatment group, however, post furosemide sodium excretion was significantly increased as compared to the controls. In the 6-OH-dopamine pretreated group furosemide did not result in an enhanced natriuresis. In spite of a comparable depletion of intrarenal neurotransmitter after 6-OH-dopamine and reserpine, the kaliuretic effect of furosemide was obviously different in both groups. Reserpine pretreatment resulted in a decrease of the kaliuretic fuorsemide effect, whereas after 6-OH-dopamine this decrease could not be observed. The post furosemide calcium excretion was significantly increased after reserpine and unchanged after 6-OH-dopamine. Basic magnesium excretion was increased by the factor 2 in both groups, as compared to the controls. Administration of furosemide completely abolished this difference.

Animals↗
PubMed1976

The influence of reserpine on the responsiveness to norepinephrine and electrolyte contents of rabbit atria.

This study was designed to investigate the relationships between reserpine-induced supersensitivity and electrolyte levels in isolated rabbit atria. Atria from reserpine-treated (1, 3 or 4 mg/kg 24 hr before) and untreated rabbits were placed in an isolated organ bath for determination of dose-response relationships for norepinephrine, or were used for electrolyte assay. Reserpine-treated atria had greater resting and maximum rates of beat than did untreated atria. However, the ED50 concentrations of norepinephrine producing a rate response were similar. Atria pretreated with 1 or 3 mg/kg reserpine were supersensitive to the inotropic effect of norepinephrine. 4 mg/kg reserpine did not induce inotropic supersensitivity. Atrial sodium contents were significantly increased by 3 mg/kg reserpine. Potassium contents were increased by 1 and 4 mg/kg reserpine. Calcium contents were significantly decreased by 4 mg/kg reserpine, while magnesium contents were increased by 1 and 4 mg/kg. Reserpine induced supersensitivity to the inotropic effects of norepinephrine but did not alter the sensitivity to the chronotropic effect of the drug. This supersensitivity may be linked to alterations in the tissue's homeostatic mechanisms for calcium.

Animals↗
PubMed1976

Association between the increase of cAMP content and the trans-synaptic induction of tyrosine hydroxylase in rat adrenal medulla. Studies with dexamethasone and reserpine.

When dexamethasone 0.25 or 2.5 mumole/kg i.p. was injected 2 h before reserpine (16 mumol/kg i.p.) the time course of the increase in cAMP content of rat adrenal medulla was changed. Reserpine alone caused a monophasic increase lasting between 1-2 h; reserpine after dexamethasone caused a biphasic increase: the immediate response, lasting between 15 and 30 min, was followed by a secondary increase beginning 2-3 h after reserpine and lasting for several hours. The overall increase in cAMP content elicited by reserpine during the 8 h following injection remained unchanged or was even increased, depending on the dose of dexamethasone. Pretreatment with dexamethasone, which delayed the increase in cAMP, also delayed the activation and translocation of protein kinase and the induction of tyrosine hydroxylase caused by reserpine in adrenal medulla. The action of reserpine on the cAMP content of adrenal medulla required an intact innervation and did not appear to be related to increased secretion of ACTH from pituitary. In denervated adrenals reserpine failed to increase the cAMP content of the medulla but not that of the cortex.

Adrenal Cortex↗
PubMed1976

Serum glucose, serum free fatty acids and adipose tissue lipids after fatal hypothermia of cold acclimatized, reserpine or propranolol treated guinea-pigs.

Surviving ability in frost (-20 degree C) was studied in cold acclimatized guinea-pigs given either reserpine, propranolol or saline. Survival time, rectal temperature at death, serum glucose, serum FFA and triglycerides in the interscapular adipose tissue were determined. Rectal temperature was highest in the reserpine group, in the same animals that endured the frost the shortest time. The survival time had decreased by about a half of that in the controls. Propranolol treatment decreased the living time only slightly. The fact that serum glucose remained high in the reserpine treated animals was obviously related to the short survival time. In the propranolol group glucose values were somewhat higher than in the control group (saline-animals). Reserpine seemed to have inhibited the release of FFA in the warm-acclimatized animals as interpreted from the low serum values. On the other hand, FFA were rather high in the cold-acclimatized reserpine animals. The blocking effect of reserpine reflected also in the higher contents of triglycerides in the adipose tissue both in cold-acclimatized and warm-acclimatized animals. Propranolol prevented slightly the depletion of the triglycerides. Amount of total lipids in the adipose tissue was lower in the cold-acclimatized animals than in the warm-acclimatized ones because of the change of the type of the adipocytes from unilocular to multilocular. The results corroborated the importance of FFA for longer survival in severe cold. Sensitization to reserpine seems to develop during cold-acclimatization. It calls attention to a possible hazard of reserpine treatment in cold environment.

Acclimatization↗