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PubMed1986

Reserpine-induced alterations in the processing of proenkephalin in cultured chromaffin cells. Increased amidation.

We have used antisera directed towards eight different portions of the proenkephalin molecule to examine the processing rates and patterns of proenkephalin-derived peptides in chromaffin cell cultures in the presence and absence of reserpine. Reserpine treatment produced profound effects on the molecular weight profile of nearly all enkephalin-containing peptides. Increased production of low molecular weight immunoreactive [Met5]enkephalin, [Leu5]enkephalin, [Met5]enkephalin-Arg6-Gly7-Leu8, and [Met5]enkephalin-Arg6-Phe7 was observed in reserpine-treated cultures; immunoreactivity corresponding to several intermediate sized enkephalin-containing peptides such as Peptide B and the high molecular weight [Met5]enkephalin-Arg6-Gly7-Leu8 immunoreactive peptide was decreased. The production of two amidated opioid peptides, amidorphin and metorphamide, was greatly accelerated in the presence of reserpine. The increased levels of low molecular weight enkephalins could not be accounted for by assuming decreased basal release. These results indicate that reserpine treatment is able to increase the extent of post-translational processing of proenkephalin within chromaffin cells.

Adrenal Medulla↗
PubMedDate not supplied

Determination of reserpine in commercial tablets by liquid chromatography with fluorescence detection.

A procedure is presented for the determination of reserpine in commercial tablets by liquid chromatography (LC). The sample is extracted with methanol if only reserpine is present. If the sample contains other ingredients, CHCI3 is used for extraction from aqueous suspension; the CHCI3 is subsequently completely evaporated in the presence of methanol. For LC, a normal phase column, methanol as the eluting solvent, and a fluorometric detector are used. A recovery study indicated that no measurable degradation of reserpine occurs during evaporation of the CHCI3 extract. Several commercial tablets containing reserpine alone or in combination with other ingredients were analyzed by the proposed method, and the results were compared with those obtained by the current official USP methods for reserpine.

Chromatography, Liquid↗
PubMed1977

The influence of reserpine and ethylenediaminetetraacetic acid (EDTA) on serotonin storage organelles of blood platelets.

The present investigation has evaluated the influence of reserpine on the serotonin-rich organelles bodies) in platelets from dogs, rabbits, and humans. Reserpine markedly depresses the levels of stored serotonin in human and animal platelets, accompanied by a small decrease in platelet ATP but no change in platelet ADP content. Thin sections of human platelets showed no change in the number or morphology of serotonin storage organelles during reserpine therapy, whereas a profound decrease in the size and number of dense bodies occurred in platelets from rabbits treated with reserpine. Dog platelets also showed a decrease in the number and density of serotonin storage organelles after reserpine therapy. The basis for the difference between rabbit and human platelets was explored by fixing platelets in glutaraldehyde and osmium in the presence or absence of the chelating agent ethylenediaminetetraacetic acid (EDTA). Most of the dense bodies in fixed human platelets were removed by EDTA while rabbit platelet dense bodies remained essentially intact. The results suggested that the opacity of rabbit platelet dense bodies following fixation with glutaraldehyde and osmium relate primarily to their serotonin content, while the electron density of human serotonin storage organelles in fixed cells is due primarily to their calcium content. Further confirmation of this concept came from studies of platelets using the whole mount technique. Rabbit platelet serotonin storage organelles were found to lack the inherent opacity of the human dense bodies, a finding consistent with the lower concentration of calcium in the rabbit organelles.

Animals↗
PubMed1985

Reserpine changes the dynamic state of enkephalin stores in rat striatum and adrenal medulla by different mechanisms.

The administration of reserpine increases enkephalin content in rat striatum and adrenal medulla. In order to investigate the mechanisms operative in this increase, we have studied in vivo the dynamic state of enkephalin stores by determining the content of proenkephalin mRNA, enkephalin precursors, and enkephalins in rats receiving reserpine. We measured proenkephalin mRNA by using a cDNA probe for human proenkephalin mRNA which hybridizes to the same species of mRNA either in the brain or in adrenal medulla. (Met5)-Enkephalin-Arg6-Phe7, as well as the high and low molecular weight forms of the enkephalins separated by Sephadex G-75 column chromatography, were measured by radioimmunoassay. Reserpine (2 mg/kg, i.p., repeated daily for two consecutive days) led 3 to 5 days later to an increase in the striatal content of proenkephalin mRNA as well as high and low molecular weight peptides containing enkephalin. The same treatment produced, in adrenal medulla, a shift from higher molecular weight to lower molecular weight enkephalin-containing peptides, an increase of enkephalin peptides, and a decrease of proenkephalin mRNA content. The results in striatum suggest that reserpine increases enkephalin synthesis by removing a tonic dopaminergic inhibition: those in adrenal medulla indicate that reserpine causes an accumulation of enkephalins by blocking the release and/or increasing the processing which may trigger a feedback-regulatory mechanism leading to a decrease in proenkephalin mRNA content.

Adrenal Medulla↗
PubMed1985

Effect of denervation and/or reserpine-induced changes on adrenomedullary catecholamines in pigeon: a fluorescence histochemical study.

Splanchnic denervation of the left adrenal gland was made in adult pigeons of both sexes. Denervation of the adrenal medulla alone did not produce any appreciable change in adrenomedullary catecholamine fluorescence in pigeon. Reserpine, at the doses of 0.05 mg, 0.2 mg and 0.8 mg/100 gm body weight was injected in both innervated and denervated pigeons. Reserpine, at all doses, induced catecholamine fluorescence depletion from the innervated pigeon adrenal medulla. Denervation failed to affect reserpine-induced epinephrine depletion while it prevented reserpine-induced norepinephrine depletion only at a low dose of reserpine.

Adrenal Medulla↗
PubMed1976

Possible involvement of a transmitter different from norepinephrine in the residual responses to nerve stimulation of the cat nictitating membrane after pretreatment with reserpine.

Pretreatment with reserpine (0.3 or 3 mg/kg, 24 hours before the experiment) reduced the norepinephrine (NE) levels in the medial muscle of the cat nictitating membrane to approximately 2% of the control values. Under these experimental conditions, the responses to postganglionic nerve stimulation were not abolished, reaching up to 50% of the maximum development of tension to exogenous sympathomimetic amines both in vivo and in vitro. In contrast to the responses to nerve stimulation obtained in normal nictitating membranes, the residual responses to nerve stimulation obtained after pretreatment with reserpine were not blocked by phentolamine (3.1 and 31 muM) or by 0.29 muM phenoxybenzamine. The effectiveness of phentolamine and phenoxybenzamine in blocking responses to exogenous NE was the same when the normal nictitating membrane was compared to the smooth muscle obtained from cats pretreated with reserpine. The residual responses to nerve stimulation were reduced when the calcium concentration in the medium was decreased to 0.65 mM. These residual responses were abolished in the presence of tetrodotoxin. Scopolamine, 0.078 muM, did not reduce the residual responses to nerve stimulation while it antagonized the responses to exogenous acetylcholine, indicating that a cholinergic mechanism is not involved in this phenomenon. Adenosine triphosphate (ATP) and adenosine diphosphosphate (ADP) behaved as agonists on the smooth muscle of the normal and of the reserpine-pretreated nictitating membrane and the responses to ATP were not blocked by phentolamine. It is concluded that the residual responses to nerve stimulation obtained after pretreatment with reserpine could be due to the release of a transmitter different from NE. The possibility that ATP or ADP might be involved in these residual responses to nerve stimulation is discussed.

Adenosine Triphosphate↗
PubMedDate not supplied

[Results of treatment of Cushing's syndrome with chloditane and large doses of reserpine].

To inhibit corticotropic function of the pituitary and glucocorticoid function of the adrenal cortex in the treatment of 41 patients with Icenko-Cushing's disease, use was made of the steroidogenesis inhibitor chloditane and high doses of reserpine. The treatment data were compared to the effect of chloditane alone in 40 patients. Inclusion of reserpine into the complex of therapeutic measures led to an appreciable decrease in corticotropin secretion which increased again shortly after the drug discontinuation. The clinical results of the treatment were comparable to those attained with administration of chloditane alone. The majority of patients manifested recurrent disease 3 to 12 months after the treatment was discontinued. Therefore, administration of reserpine as an additional means in the treatment was discontinued. Therefore, administration of reserpine as an additional means in the treatment of Icenko-Cushing's disease by chloditane with a view of a steady inhibition of corticotropic function of the pituitary and the prophylaxis of recurrencies is not desirable. High doses of reserpine may be recommended at the initial stages of the disease treatment in the presence of an extremely high level of blood plasma corticotropin.

17-Hydroxycorticosteroids↗
PubMed1983

Antagonism by tricyclic antidepressants of reserpine-induced hypothermia in mice. Involvement of postsynaptic alpha 2-adrenoceptors.

The effects of adrenoceptor blocking agents and cyproheptadine on the antagonism by the antidepressants imipramine, desipramine and maprotiline, of reserpine-induced hypothermia in mice were studied. The anti-reserpine effect of the antidepressants was reduced by phenoxybenzamine, prazosin, yohimbine and d,1-propranolol, the two latter drugs exhibiting the strongest effect. Practolol was ineffective, while cyproheptadine potentiated the effect of maprotiline and was inactive towards imipramine and desipramine. Furthermore, the anti-reserpine effect of desipramine (the other antidepressants not being studied) was also reduced by piperoxan and l-propranolol, but not by d-propranolol. The reserpine-induced hypothermia was antagonized by clonidine and this effect was completely blocked by yohimbine and partly reduced by prazosin. These results confirm that the antagonism by tricyclic antidepressants of reserpine-induced hypothermia depends on the activation of noradrenergic mechanisms and indicate that this effect is mediated not only by alpha 1- and beta-, but also by postsynaptic alpha 2-adrenoceptors.

Animals↗
PubMed1978

Reserpine-induced supersensitivity to the chronotropic and inotropic effects of calcium in rabbit atria.

Supersensitivity to the chronotropic and inotropic effects of calcium was demonstrated in spontaneously beating paired atria from reserpine-pretreated (0.1 mg/kg/day, 7 days) rabbits. Supersensitivity to the inotropic effects of calcium in electrically driven left atria was also demonstrated. Atria were driven at 80, 100 and 120 beats/min. At each frequency the reserpine-pretreated atria were more sensitive than controls. Atria were tested under diastolic tensions of 1,2 and 4 g. As the tension was increased the sensitivity to calcium increased. The sensitivity of reserpine-pretreated atria was greater at each tension than that of control atria. Atria tested at 37 degrees C were less sensitive than those tested at 30 degrees C; however, the reserpine-pretreated atria were more sensitive than control atria at both temperatures. This study demonstrates that reserpine-induced supersensitivity to the inotropic effects of calcium can be obtained and that the ability to demonstrate this phenomenon does not appear to be altered by the frequency, diastolic tension or temperature at which each experiment is performed.

Animals↗
PubMed1984

Diltiazem for treatment of essential hypertension: a double-blind controlled study with reserpine.

In a double-blind, parallel, 12-week trial, antihypertensive effects of diltiazem and reserpine were compared in 107 patients with essential hypertension. Diltiazem reduced blood pressure from 176/100 mmHg to 154/86 mmHg after 12 weeks, and reserpine reduced blood pressure from 171/96 mmHg to 155/85 mmHg. The difference between diltiazem and reserpine was not statistically significant. However, among a subset of patients given 180 mg/day of diltiazem, a significantly better antihypertensive effect was achieved than among a subset given 0.3 mg of reserpine. The incidence of side effects and complications in the diltiazem group was about one half that in the reserpine group (12.3% and 27.1%, respectively). Side effects of diltiazem were mild, and the drug was extremely well tolerated. These results show that diltiazem is an effective antihypertensive drug for the treatment of mild to moderate essential hypertension.

Adult↗
PubMed1983

Studies on the photostability of reserpine in parenteral solutions.

The photostability of reserpine in several parenteral formulations has been studied and the effects of some commonly used stabilizers have been evaluated. The kinetic data indicate that the photodegradation of reserpine follows zero order kinetics in all the formulations at pH = 2 and 3. The stability of reserpine appears to be higher at pH = 3 than at pH = 2. 3-dehydroreserpine, isoreserpine and lumireserpine were identified as the major photodegradation products by TLC, suggesting that the photodegradation in acidic solutions occurs initially via an oxidative mechanism. The combined effect of EDTA and PABA on the photostability of reserpine was more significant than their individual effect. The formulations in which benzyl alcohol was used as vehicle were found to be more stable than those having propylene glycol. Polyethylene glycol was found to be a better surfactant than Tween 80. The degree of stabilization in the presence of surface active agents has been explained in terms of micellar theory and the degree of hydration of micelles. A stable formula for parenteral solution of reserpine has been suggested.

4-Aminobenzoic Acid↗
PubMed1983

Enhancement of the release reaction not accompanied with enhanced phosphatidylinositol turnover in the reserpinized rabbit blood platelets.

Thrombin-induced platelet release reaction examined with secretion of calcium and N-acetylglucosaminidase was significantly enhanced in the platelets from reserpine-treated rabbits as compared with the control. On the other hand, 32P-incorporation into phosphatidic acid was suppressed in the reserpinized platelets in activated state. Thrombin induced phosphatidylinositol (PI)-breakdown, which was examined by decreases in radioactivity and content of PI, and an increase in diacylglycerol, was not enhanced in the reserpinized platelets as compared with the control. The phosphorylation of the specific protein coupled to thrombin-induced platelet PI-breakdown was not stimulated in the reserpinized platelets as compared with the control. In contrast to PI, PC-degradation by thrombin was significantly stimulated in the reserpinized platelets. Possible existence of pathway(s) other than that associated with an enhancement of PI-turnover is conceivable as a mechanism involved in platelet release reaction.

Acetylglucosaminidase↗
PubMed1983

Reserpine and carcinogenesis: inhibition of carcinoma formation in mice.

Long-term administration of reserpine, an alkaloid, significantly retarded the induction of squamous cell carcinomas by a chemical carcinogen, 3-methylcholanthrene (MCA) in Swiss male albino mice. The incidence and development of carcinomas in mice simultaneously treated with reserpine and MCA was notably lowered as compared to those occurring in mice treated with MCA alone at any time interval. DNA synthesis and the percentage of labeled cells with [3H]thymidine was also significantly decreased in the nuclei of tumor cells following reserpine and MCA administration as compared to the findings for cells treated with MCA alone (18.50 and 39.00%, respectively). Electron microscopic and cytologic observations of tumors revealed the predominance of large areas of cytolysis and disintegration with an increase of lysosomes, myelin figures, and a decrease of mitochondria and polyribosome populations in tumor cells treated with reserpine and MCA, as compared to those results after treatment with MCA only. These findings demonstrate that reserpine significantly inhibited the carcinoma induction by a chemical carcinogen (MCA) in mice, possibly by inducing an advanced cytolysis and decreasing DNA synthesis in mouse tumor cells.

Animals↗
PubMed1984

Reserpine binding to bovine chromaffin granule membranes. Characterization and comparison with dihydrotetrabenazine binding.

[3H]Reserpine bound reversibly in vitro to chromaffin granule membranes. Binding was temperature-dependent and slow, and had biphasic kinetics. The addition of ATP accelerated the kinetics, which became monophasic and comparable to those of [3H] dihydrotetrabenazine, without affecting the binding equilibrium constants. The ATP effect was related to H+ -electrochemical gradient generation by the granule membrane H+ pump. Binding of reserpine to chromaffin granule membranes occurred on two classes of sites: R1, Bmax = 7 pmoles/mg of protein and KD = 0.7 nM, and R2, Bmax = 60 pmoles/mg of protein and KD = 25 nM. Sites R2 were considered to be equivalent to [3H] dihydrotetrabenazine binding sites, as the densities of the R2 and the [3H] dihydrotetrabenazine binding sites were similar and because tetrabenazine displaced reserpine from R2 sites. Sites R1 were tetrabenazine-resistant; they were involved in monoamine uptake, since their KD values were similar to the KI values of reserpine for noradrenaline uptake. Sites R1 were less abundant than sites R2 on chromaffin granule membranes, but they were present at the same concentration in intact chromaffin granules. We propose that the monoamine carrier exists in two forms: (a) an active form bearing both high- and low-affinity sites for reserpine and (b) an inactive form with only the low-affinity R2 sites.

Adrenal Medulla↗
PubMed1984

Effects of reserpine on prolactin levels and incidence of breast cancer in postmenopausal women.

Epidemiological studies of reserpine use and breast cancer have generally found only small increases in breast cancer risk, even after long-term use. Prolactin levels in short-term reserpine users have been reported to be in the range of those of lactating women, levels which rodent experiments suggest should greatly increase breast cancer incidence. We measured prolactin levels in 15 women who had been taking reserpine-containing drugs for at least 5 years and compared them to levels in 15 women taking non-reserpine-containing antihypertensives and 15 women taking no antihypertensive medicines. Although reserpine users had significantly elevated levels of prolactin, their mean level was only approximately 50% greater than the mean level of the combined results from the two control groups. Based on a statistical model of breast cancer incidence, we calculate that such increases in prolactin in the postmenopausal period would be likely to cause only small increases in breast cancer risk, as have been observed in epidemiological studies.

Aged↗
PubMed1982

Low doses v standard dose of reserpine. A randomized, double-blind, multiclinic trial in patients taking chlorthalidone.

Reserpine in different doses was assigned in random, double-blind fashion to 329 patients with mild to moderate hypertension who had not achieved normotension with chlorthalidone therapy alone. The additional reduction of BP averaged 11.0/10.4 mm Hg with chlorthalidone, 50 mg, plus reserpine, 0.25 mg (C 50+R 0.25); 9.5/9.4 mm Hg with C 50+R 0.125; 6.4/8.5 mm Hg with C 50+R 0.05; and 9.9/9.6 mm Hg with C 25+R 0.125. The percentage of patients in whom control was achieved at diastolic BP less than 90 mm Hg and at least 5 mm Hg below baseline with either chorthalidone alone or with reserpine added was 65% with C 50+R 0.25, 69% with C 50+R 0.125, 58% with C 50+R 0.05, and 56% with C 25+R 0.125. Side effects of lethargy and impotence noted by patients with the 0.05-mg dose of reserpine were only one third of those noted with the 0.25-mg dose, although the incidence of other side effects did not differ. These results indicate that hypertension in many persons can be controlled by less than customary doses of reserpine in combination with a diuretic.

Blood Pressure↗
PubMed1981

Effect of reserpine pretreatment on in vivo femoral arterial responses to vasodilator agents.

This study determined the effects of reserpine pretreatment (1 mg/kg i.m., 24 hr before) on in vivo femoral arterial responses in the dog to the vasodilator agents acetylcholine, isoproterenol, dibutyryl cyclic AMP, adenosine, nitroglycerin and hydralazine. Femoral blood flow was monitored from the right femoral artery into which i.a. injections of the vasodilator agents were given just distal to the flow probe. Femoral vascular resistance was calculated as the ratio of mean systemic blood pressure to femoral blood flow. The response to each dose of vasodilator agent was evaluated by the magnitude of the slope of the regression line relating the resultant decrease in resistance to the resistance before the injection. Reserpine pretreatment increased slopes of these regression lines for adenosine, nitroglycerin, acetylcholine and isoproterenol, suggesting a general enhancement of vasodilator responses by reserpine. Both hydralazine pretreatment (1 mg/kg i.v., 1 hr before testing) and partial aortic occlusion during testing decreased femoral perfusion pressure without increasing vasodilator responses of the femoral arterial bed to adenosine, nitroglycerin, acetylcholine or isoproterenol. Therefore, the enhancement of vasodilator responses by reserpine was apparently not a result of decreased femoral perfusion pressure due to reserpine.

Acetylcholine↗
PubMed1982

[Gastric movements and reserpine-induced ulcer in rats].

Changes of gastric movements and ulcerogenic mechanisms in reserpine (6 mg/kg s.c.)-induced ulcer were studied in Wistar male rats weighing 180 to 220 g after fasting for about 20 hr. Under anesthesia with Nembutal (30 mg/kg i.p.), rats were fixed on their backs. The abdomen was incised and the stomach was exposed. Gastric movements of the fundic glandular area of greater curvature (A), the fundic-antral area of lesser curvature (B), and the neighboring area of pylorus (C) were recorded electromyographically after placing a small bipolar electrode of 1 mm distance on each area. Spontaneously, many higher amplitudes were found in area B and less found in area A. In area C, there were the least number of spikes and the lowest amplitudes. These gastric movements were inhibited until 1 hr after reserpine followed by a gradual increase in spikes and higher amplitudes. This increase was long-lasting and most marked in area B. Increased gastric movements due to reserpine were completely inhibited by atropine and vagotomy, moderately inhibited by hexamethonium and diphenhydramine, and only weakly inhibited by l-phenylephrine, l-isoproterenol, phentolamine, propranolol, metiamide, and methysergide. In reserpine-induced ulcer, ischemia occurred most markedly in area A, but erosions initiated from area B as reported previously. In area B, the gastric movements were most active, and the erosions were inhibited by the drugs which suppress gastric movements. These results suggest that reserpine-induced ulcer is due not only to the ischemia in the earlier stage, but also to the long-lasting hypermotility in the later stage.

Animals↗