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PubMed1957

Intraventricular administration of reserpine and its metabolites to conscious cats.

Intraventricular injection of reserpine in conscious cats produced relaxation of the nictitating membrane, miosis with narrowing of the palpebral fissure to a slit, avoidance of light, diarrhoea, anorexia, and tranquillization. Equivalent doses of trimethoxybenzoic acid, reserpic acid or methylreserpate separately or in combination did not produce such effects, indicating that these reserpine metabolites were not involved in these reserpine actions. 5-Hydroxytryptamine alone or in combination with subthreshold doses of reserpine also did not duplicate the effects observed after effective doses of reserpine. The possible central sites of reserpine action are discussed.

Animals↗
PubMed1961

The effect of mephentermine on isolated dog hearts, normal and pretreated with reserpine.

The inotropic activity of the non-catechol sympathomimetic amine, mephentermine sulphate, on the failing dog heart-lung preparation, was 1/10 to 1/20 that of adrenaline. Mephentermine showed no inotropic effect on preparations from animals pretreated with reserpine. The chronotropic and "calorigenic" actions of mephentermine were tested on modified heart-lung preparations to permit a more accurate measurement of coronary flow, and were found to be greater than its inotropic effect relative to adrenaline. Furthermore, the action of mephentermine was longerlasting than that of adrenaline. If adrenaline was infused 15 min after the termination of mephentermine administration and when the action of the latter was still at a maximum, a further increase in heart rate and especially oxygen consumption was observed. In preparations from dogs treated with enough reserpine to deplete the heart of noradrenaline, mephentermine had only slight chronotropic and calorigenic actions. However, further addition of adrenaline after a 15 min pause caused a rise in heart rate, oxygen consumption, and coronary flow which almost duplicated the additive effects of both amines on the preparations not treated with reserpine. It would appear that adrenaline acted on its own and in addition "restored" the action of mephentermine on the reserpinized preparations. The action of adrenaline alone on reserpinized preparations was not increased compared with that on normal preparations. These observations are relevant to a consideration of the mechanism of action of non-catechol sympathomimetic amines on the heart, and are in harmony with the concept that mephentermine, a non-catechol amine, requires the presence of added or stored catechol amines for its action. Reserpine treatment did not alter the mechanical efficiency of the heart despite its depletion of noradrenaline.

Amines↗
PubMed1969

Effect of reserpine on the subcellular distribution of 3H-alpha-methylnoradrenaline in the mouse heart.

1. Mice were injected with reserpine (0.5 mg/kg or 2.5 mg/kg) at various intervals after an intravenous injection of (3)H-alpha-methylnoradrenaline ((3)H-alpha-MeNa), 20 mug or 100 mug/kg. The effect of reserpine on the content of labelled amine in the subcellular fractions of the heart was studied.2. In most experiments reserpine caused a pronounced decrease in the (3)H-alpha-MeNA content of the particulate fraction (P). The decrease was most pronounced when the higher dose of reserpine and lower dose of alpha-MeNA were used. In most experiments, the (3)H-alpha-MeNA content of the supernatant fractions was unchanged and, therefore, the P/(P + S) ratio was decreased.3. It is concluded that the effect of reserpine is a releasing effect on the particulate (granular) fraction, probably by blocking the re-uptake of the amine leaked from the granules. No support was found for the hypothesis that reserpine acts by inhibition of release of amines from the nerve granules.

Animals↗
PubMed1973

The effects of (-)-delta9-tetrahydrocannabinol on reserpine-induced hypothermia in rats.

1. An intravenous injection into rats of 1 mg/kg (-)-Delta(9)-tetrahydrocannabinol Delta(9)-THC) had no effect on rectal temperature and produced in the subcellular fractions of the brain a shift of 5-hydroxytryptamine (5-HT) from the particulate or ;bound' 5-HT to the supernatant or ;free' fraction, whereas the noradrenaline (NA) decreased in both fractions.2. Pretreatment of rats by an intravenous injection of 1 mg/kg Delta(9)-THC three times a week for four weeks, prevented the hypothermia and the reduction in brain 5-HT produced by an intraperitoneal injection of 15 mg/kg reserpine given 24 h after the last Delta(9)-THC injection.3. Pretreatment of rats by a single intravenous injection of 1 mg/kg Delta(9)-THC prevented the hypothermia and reduction in brain 5-HT produced by an intraperitoneal injection of reserpine given 1 h before. The reduction in brain NA was not prevented except at the 18 h time interval.4. An injection of 1 mg/kg Delta(9)-THC intravenously into rats 3 h after an intraperitoneal injection of reserpine accentuated the reserpine hypothermia as well as the reduction of 5-HT but not of NA in the brain.5. The reserpine hypothermia was not prevented by a single intravenous injection of 1 mg/kg Delta(9)-THC when cinanserin, a 5-HT inhibitor, was injected 30 min before the reserpine.

Anilides↗
PubMed2005

Evidence for a reserpine-affected mechanism of resistance to tetracycline in Neisseria gonorrhoeae.

The presence of a reserpine-affected mechanism of tetracycline resistance was investigated in 17 Neisseria gonorrhoeae clinical isolates. To establish this fact the MIC of tetracycline in the presence and absence of reserpine was determined, and, in addition, mechanisms of tetracycline resistance were analyzed by PCR. The results showed that reserpine affects the MIC of tetracycline at least 4-fold in all isolates, including those containing the tetM gene. An inhibitory effect of reserpine against the MtrCDE efflux system was ruled out by using strains either with an inactive or with an unrepressed MtrCDE system. The results suggest the presence of a constitutive system of resistance to tetracycline, by a possible efflux pump, which may be inhibited by reserpine. Further studies are required to determine the exact nature of the action of reserpine on the MIC of tetracycline.

Anti-Bacterial Agents↗
PubMed1968

Temperature effects of reserpine injected into the cerebral ventricles of rabbits and cats.

1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.2. In rabbits the reserpine (0.5-0.6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.3. In cats the reserpine (0.5-0.75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic fibres ending at these cells. When these fibres are depleted of their noradrenaline by one or two injections of reserpine, these effects are not obtained because noradrenaline is no longer available to be released in sufficient amounts to raise temperature in rabbits and to lower it in cats.

Animals↗
PubMed1979

Effects of noradrenaline and metaraminol on isolated aortic strips and auricles obtained from untreated and reserpine-treated rabbits.

The isolated aortic strips of the untreated rabbits responded to noradrenaline in concentrations ranging from 20 to 160 ng/mL, whereas similar preparations from reserpine-treated animals responded to lower concentrations (from 2.5 to 10 ng/mL) and larger effects were produced by concentrations ranging from 20 to 160 ng/mL. Comparatively stronger concentrations (from 0.4 to 1.6 microgram/mL) of metaraminol were required to produce suitable contractile responses, which were not modified by reserpine pretreatment. On the isolated auricles obtained from untreated rabbits, noradrenaline was used in concentrations of 20 and 80 ng/mL, but these concentrations were reduced to 2.5 and 10 ngmL in the case of tissues obtained from reserpinized rabbits. Comparatively stronger (0.2 and 0.8 microgram/mL) concentrations of metaraminol were required to produce a stimulant effect on this preparation, and the sensitivity was not altered by reserpine pretreatment. These observations lead to the conclusions that though reserpine pretreatment produces a well-marked increase in the sensitivity of isolated rabbit aortic strips and auricles to noradrenaline, it does not modify the sensitivity of these preparations to metaraminol. Reserpine was used in 0.3 mg/kg doses injected subcutaneously for 3 successive days.

Animals↗
PubMed1981

Intestinal secretion of mucin in chronically reserpine-treated rats.

Intestinal glycoprotein synthesis and secretion were measured in vivo and in vitro in rats treated for 7 days with reserpine. Goblet cell mucin was measured by radioimmunoassay. Reserpine-treated rats contained 1.4 times more mucin in intestinal tissue than control rats (P less than 0.05) and incorporated [1-14C]glucosamine in vivo at 1.52 times the rate of controls (P less than 0.01). Intestinal slices incubated for 90 min in vivo incorporated 1.4 times more [14C]glucosamine (P less than 0.001) and 3.0 times more [3H]threonine (P less than 0.01) into protein of reserpine-treated tissue than controls. The extra 14C was localized to mucin and to smaller components that had affinity for Concanavalin-A-Sepharose, did not bind to mucin antibody, and were therefore nonmucin glycopeptides. In vitro secretion of mucin was three times greater for reserpine-treated tissue than for control tissue (P less than 0.0001). There was an impairment in the mucin secretory response of reserpine-treated tissue to the addition of cholera toxin. Thus, chronic reserpine treatment results primarily in a generalized increase in the rate of intestinal glycoprotein synthesis, subsequent accumulation in tissues, and an increased (but not fully proportional) secretion of mucin. We speculate that in cystic fibrosis a similar sequence of glycoprotein abnormalities may be responsible for the gradual obliteration of exocrine gland ducts with viscous mucus.

Animals↗
PubMed1985

Colonic glycoprotein secretion and calmodulin-acceptor proteins in the reserpine-treated rat.

The rate of radioactive precursor-labeled colonic glycoprotein secretion in chronically reserpine-treated versus saline-injected control rats was examined. Everted colonic sacs prepared from reserpine-treated rats were found to be hypersecretory, exhibiting a basal rate of glycoprotein secretion that was threefold higher than control everted sacs. Furthermore, glycoprotein secretion in control tissue was stimulated by the secretagogue carbachol, and this stimulation was precluded by 10 microM trifluoperazine, the calmodulin antagonist. Reserpine-treated tissue, in contrast, was refractory to treatment with carbachol as well as trifluoperazine. While reserpine-treated and control colonic mucosae were demonstrated to contain equivalent levels of calmodulin via radioimmunoassay, reserpine-treated tissue was determined to lack two calmodulin-acceptor proteins with molecular weights of 29 and 47 kilodaltons. The data suggest that the mechanism by which reserpine elicits this cystic fibrosislike, hypersecretory state of glycoprotein secretion within the colonic mucosa entails the loss of calmodulin function in the regulation of this secretory process. We speculate that the biochemical defect present in cystic fibrosis could also entail such a loss of calmodulin function in the regulation of glycoprotein secretion.

Animals↗
PubMedDate not supplied

Characteristics of (-)-stepholidine on the firing activity of substantia nigral dopamine neurons after repeated reserpine treatment.

Although (-)-stepholidine [(-)-SPD] exhibits antagonistic effects to normosensitive dopamine (DA) receptors, it shows agonistic effect (probably D1) on rotational behavior in rats with unilateral 6-OHDA lesions of substantia nigra pars compacta (SNC). In this study, another supersensitive model, reserpinized rats (1 mg/kg x 6 days, s.c.), were used to investigate the properties of (-)-SPD. In reserpinized rats, (-)-SPD reversed and/or significantly attenuated the firing inhibition caused by the mixed DA receptor agonist apomorphine (APO). After reserpinization, the selective D1 and D2 receptor agonists separately inhibited the firing rate of SNC DA neurons, and (-)-SPD reversed both D2 receptor agonist N-0437- and D1 receptor agonist SKF 38393-induced inhibition of the SNC DA cell firing. These results suggest that (-)-SPD shows D1 and D2 receptor antagonistic action and does not possess the same DA receptor agonistic effect on SNC DA cell firing activity in reserpinized supersensitive rats as it does in unilateral 6-OHDA-lesioned rotational behavior. Also, large doses of (-)-SPD inhibited the firing rate of SNC DA cells in reserpinized rats, but the inhibition was not reversed by D1 receptor antagonist SCH 23390 but was reversed by N-0437 or APO. This inhibition, thus, could be interpreted as depolarization inactivation (DI) due to blockade of DA receptors. Interestingly, in control (nonreserpinized) rats, (-)-SPD did not produce DI of SNC DA cells as it did on ventral tegmental area DA cells. These results imply that reserpinization modulates the onset of DI of SNC DA cells and that (-)-SPD may serve as a leading compound for exploring new types of atypical neuroleptics.

Action Potentials↗
PubMed1984

Function of tuberoinfundibular dopamine neurons in pargyline- and reserpine-treated rats.

The synthesis and release of dopamine within tuberoinfundibular neurons were studied in rats treated with reserpine and/or pargyline. The effect of reserpine to elevate the serum concentration of prolactin was accompanied by a 70-80% reduction in the concentration of dopamine in pituitary stalk plasma. When rats were given pargyline (75 mg/kg) prior to the administration of reserpine (2.5 mg/kg), the reserpine-induced alterations in serum prolactin and stalk plasma dopamine concentrations were completely prevented. Pargyline treatment alone resulted in a significant elevation of the concentration of dopamine in pituitary stalk plasma and a reduction in the serum concentration of prolactin. The effects of reserpine and pargyline on the synthesis of dopamine in the median eminence were found to be the opposite of their effects on the release of dopamine. Dopamine synthesis (as estimated by the accumulation of dihydroxyphenylalanine after inhibition of decarboxylase activity) was increased after reserpine and decreased after pargyline administration. Thus, these data serve to illustrate the point that, under certain conditions, the release of dopamine from tuberoinfundibular neurons can be dissociated from its rate of synthesis. More importantly, it appears the release of dopamine from these neurons is dependent upon intact dopamine storage function and monoamine oxidase activity, in addition to continued catecholamine synthesis.

Animals↗
PubMed1993

Ischemic preconditioning fails to limit infarct size in reserpinized rabbit myocardium. Implication of norepinephrine release in the preconditioning effect.

BACKGROUND: Infarct size reduction by ischemic preconditioning is believed to be mediated by adenosine; however, whether adenosine is the factor responsible for the initiation of this protection remains unknown. It is possible that during preconditioning, adenosine stimulates receptors on presynaptic nerve terminals and retards the release of norepinephrine (NE) during the prolonged ischemia or that NE release during preconditioning augments adenosine production. METHODS AND RESULTS: To test whether the release of NE is involved in the preconditioning phenomenon, rabbits were pretreated with reserpine (5 mg/kg sc, 24 hours before) to deplete presynaptic nerve terminals of NE stores. On the day of the experiment, the rabbits were anesthetized with ketamine-xylazine and instrumented for coronary occlusion. Nonreserpinized animals were used as controls. The control group (n = 7) was subjected to 30 minutes of coronary occlusion and 120 minutes of reperfusion (ischemia-reperfusion) only. The preconditioned group (n = 10) received 5 minutes of preconditioning ischemia and 10 minutes of reperfusion before the prolonged ischemia-reperfusion. Of the reserpinized animals, half (n = 7) received preconditioning before ischemia-reperfusion and the remaining animals (n = 7) did not. At termination of the experiment, an intravenous tyramine challenge (1 mg/kg) was used to confirm NE depletion in reserpinized rabbits. The resulting infarcts were measured with tetrazolium and planimetry. With comparable hemodynamics and areas at risk, infarct size in control animals was 39.8 +/- 2.1% of the risk region. Preconditioned animals showed an expected reduction of infarct size to 14.8 +/- 2.2% of risk region (P < .05 vs control). Of the reserpinized animals, those that received reserpine alone had infarcts that were 38.5 +/- 4.5% of risk region, and those that were preconditioned had infarcts that were 41.4 +/- 3.6% of risk region, which was not significantly different than the control group. CONCLUSIONS: We conclude that preconditioning fails to protect ischemic-reperfused myocardium in reserpinized rabbit myocardium, indicating that the release of NE during either preconditioning or prolonged ischemia is critical to preconditioning mediated protection.

Animals↗
PubMedDate not supplied

Reserpine and breast cancer in the Hypertension Detection and Follow-Up Program.

Recent reports on the efficacy of pharmacological management in reducing mortality associated with mild hypertension have enhanced the importance of increasing our knowledge about drug toxicity. The Hypertension Detection and Follow-Up Program (HDFP) provides a convenient setting in which to examine the association reported between reserpine usage and breast cancer. In the intensively treated and followed group (Stepped Care [SC]), the relative breast cancer experience of those who did take reserpine and those who did not was examined. Of 2529 females in SC, 1036 received reserpine, with an average exposure of 1.97 years during 5 years of follow-up. Through extensive investigation, 21 cases of breast cancer were identified. using a life table regression method of analysis to adjust for actual time of reserpine exposure, race, sex, and medication status at entry, and comparing those who took reserpine with those who did not, the author's calculated a risk ratio of 1.28, with a confidence interval of 0.58 to 2.80. Adjustment for a number of other variables known to have relationships to breast cancer did not appreciably change the results. Thus, with certain precautions, the authors conclude that in this setting there is no indication of the recently postulated association of reserpine and the short-term enhancement of breast tumor growth.

Adult↗
PubMed1975

Blockage of estrogen-induced release of luteinizing hormone by reserpine and potentiation of synthetic gonadotropin-releasing hormone-induced release of luteinizing hormone by estrogen in the ovariectomized ewe.

These experiments tested the effects of reserpine on estrogen-induced LH release and the effects of estrogen on gonadotropin-releasing hormone-induced LH release in ovariectomized ewes. Injection of 50, 200, or 500 mug of estradiol benzoate (EB) into progesterone-treated ewes, or of 50 mug of EB into non-treated ewes induced a large surge in serum LH levels approximately 15 h later. Injection of 5 mg/ewe of reserpine 6 h prior to the EB, blocked the LH surge. Reserpine reduced, but did not block the release of LH induced by injection of 20 mug or 40 mug of synthetic gonadotropin-releasing hormone (GnRH). Injection of graded doses (5, 10, or 20 mug) of GnRH into progesterone-treated ewes that had been treated with reserpine, induced increases in serum LH levels that were proportional to the logarithm of the dose. In the final series of experiments both progesterone-treated and non-treated ewes were injected with reserpine and then with either EB or oil. Fifteen hours after receiving EB or oil they were injected with either GnRH or the diluent. GnRH elevated serum LH levels significantly higher in ewes given EB than in those given oil. LH levels in ewes given oil and diluent were not elevated. These data suggest that reserpine blocked EB-induced LH release by an action on the central nervous system and that EB acted directly on the anterior pituitary to increase the response to GnRH.

Animals↗
PubMed1985

[A TRH analog (DN-1417). Antagonistic effects on reserpine-induced decreases in local cerebral glucose utilization and cerebral monoamine levels].

Thyrotropin-releasing hormone (TRH) and its analog, DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide citrate), significantly antagonized against reserpine-induced reduction of the spontaneous motor activity and the electroconvulsive threshold in mice. To search for sites of action and mechanisms, effects of DN-1417 on reserpine in local cerebral glucose utilization (LCGU) and cerebral monoamine levels were also investigated in rats. Reserpine (2 mg/kg, i.p., 24 hr pretreatment) reduced LCGU and the levels of cerebral monoamine in all the brain regions. DN-1417 (5 mg/kg, i.v.) significantly reversed the reduction of LCGU induced by reserpine in the thalamus dorsomedial nucleus, mamillary body, septal nucleus, caudate-putamen and nucleus accumbens. The effects of DN-1417 were completely abolished by pretreatment with a dopaminergic (DA) and a serotonergic (5-HT) receptor blocker, pimozide (1 mg/kg) and methysergide (5 mg/kg), respectively. DN-1417 (20 mg/kg, i.p.) reversed 5-HT level in the hypothalamus depleted by reserpine. These results suggest that the antagonistic effects of DN-1417 against reserpine-induced reduction of the locomotor activity and the electroconvulsive threshold seem to be mediated by DA- and 5-HT-ergic activations mainly in the nucleus accumbens and hypothalamus, respectively.

Acid-Base Equilibrium↗
PubMed1993

Effects of reserpine treatment on pituitary-adrenocortical axis in patients with Cushing's disease.

Effects of reserpine treatment, not associated with pituitary irradiation, on the pituitary-adrenocortical axis in a total of 37 untreated patients with Cushing's disease were evaluated. With short-term treatment (2 mg daily for 2 weeks, n = 36), basal excretion of urinary 17-OHCS significantly decreased from 11.2 +/- 5.2 mg/day/m2 (body surface area) (mean +/- SD) to 9.6 +/- 4.4 mg/day/m2 (P < 0.01), and metyrapone-induced incremental responses of urinary 17-OHCS decreased from 58.4 +/- 41.4 mg/3 days/m2 to 45.9 +/- 29.8 mg/3 days/m2 (P < 0.05). Long-term treatment (1.7 +/- 0.3 mg/day for a mean of 15.8 +/- 19.9 weeks) induced a marked reduction in plasma cortisol, and 24-h urinary 17-OHCS and/or free cortisol in 4 of 8 patients examined. Long-term reserpine administration caused normal suppression of plasma cortisol (or 11-OHCS) in 3 of 9 patients with 1 mg, and in all of 5 patients with an 8 mg overnight dexamethasone suppression test. Plasma ACTH response to CRH was evidently decreased in one patient evaluated one month after the initiation of reserpine. The circadian rhythm of plasma cortisol was normal in one patient when the basal glucocorticoid level became normal with reserpine treatment. The present findings suggest that reserpine itself contributes in a causal fashion to the effectiveness of our regimen, reserpine and pituitary irradiation, for some Cushing's disease patients in whom it is effective.

17-Hydroxycorticosteroids↗
PubMed1994

Hyperresponsiveness of cardiac muscles to histamine in reserpine-treated guinea pigs.

The hyperresponsiveness of cardiac tissue to histamine following treatment with reserpine was pharmacologically characterized. Guinea pig hearts were isolated 24 hours after intraperitoneal administration of 5 mg/kg reserpine. This treatment resulted in a complete depletion of tissue norepinephrine. Reserpine treatment potentiated the positive inotropic response of isolated perfused hearts to histamine at doses ranging from 0.3 to 3 micrograms (23 to 57% increase for reserpine-treated animals vs. 14 to 32% increase for control animals). Isolated left ventricular papillary muscle of reserpine-treated guinea pig hearts also showed hyperresponsiveness to histamine at concentrations of 0.1 microM or greater. The hyperresponsiveness of the papillary muscle contraction of the reserpine-treated animals to histamine was abolished in the presence of 1 microM cimetidine, but not attenuated in the presence of 1 microM diphenhydramine. This hyperresponsiveness was not modified by 1 microM bunazosin or 1 microM propranolol. The results suggest that H2-receptor mediated action plays a role in the hyperresponsiveness of cardiac muscles to histamine.

Animals↗
PubMed2000

Collaborative work to evaluate toxicity on male reproductive organs by repeated dose studies in rats 8). Effects of daily subcutaneous administration of reserpine on spermatogenesis for 2 and 4 weeks.

To obtain information on the validity and the limitations of 2-weeks repeated-dose toxicity studies to detect effects on the male genital organs of rats, reserpine was administered daily at 0.05 and 0.1 mg/kg by subcutaneous injection to Crj:CD(SD)IGS male rats for 2 and 4 weeks (2-weeks and 4-weeks studies). In the 2-weeks study, suppression of body weight gain was observed in the reserpine 0.1 mg/kg group. In the 4-weeks study, suppression of body weight gain and a decrease in prostate weight were observed in the reserpine 0.1 mg/kg group. Slight to moderate retention of step 19 spermatids in the seminiferous tubules (stages IX-XI) was observed in a few animals of both the reserpine 0.05 and 0.1 mg/kg groups in both the 2- and 4-weeks studies. However, seminiferous tubule atrophy with degeneration of germ sells was observed sporadically not only in the reserpine groups but also in the control group, and this change might have been the cause of the spermatid retention. Therefore, we were unable to reach a clear conclusion with regard to whether it is possible to detect reserpine toxicity on spermatogenesis in rats after 2-weeks administration.

Animals↗