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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↗
PubMed1985

Reevaluation of reserpine-induced suppression of contact sensitivity. Evidence that reserpine interferes with T lymphocyte function independently of an effect on mast cells.

It has been suggested that reserpine blocks expression of delayed hypersensitivity (DH) by depleting tissue mast cells of serotonin (5-HT), thereby preventing a T cell-dependent release of mast cell 5-HT necessary to localize and to amplify the DH response. However, reserpine blocks expression of DH in mast cell-deficient mice. We therefore decided to reevaluate the mechanism by which reserpine abrogates expression of cellular immunity, and investigated whether the drug might interfere with T cell activity in vitro or in vivo. At concentrations as low as 4 microM, reserpine profoundly suppressed baseline or antigen-augmented levels of [3H]thymidine incorporation by immune lymph node cells obtained from mice sensitized to the contactant oxazolone [I-LNC(Ox)]. This effect was observed both with I-LNC derived from normal mice and with I-LNC derived from congenitally mast cell-deficient W/Wv mice, cell preparations that lacked detectable mast cells, histamine, and 5-HT. Furthermore, treatment of I-LNC with reserpine (20 microM) for 1 h in vitro virtually abolished the ability of these cells to transfer CS to naive mice. This was not a cytolytic effect, as the viability of the I-LNC treated with reserpine was not affected, and washing of the reserpine-treated I-LNC before transfer fully restored their ability to orchestrate a CS response. The action of the drug was not mediated by an effect on mast cells, since the experiment could be performed using mast cell-deficient W/Wv mice as both donors and recipients of I-LNC. In addition, the effect was specific for the treated cells: mice that received reserpine-treated I-LNC(Ox) intravenously together with untreated I-LNC(DNFB) did not develop CS to Ox but responded normally to DNFB; and local intradermal injection of reserpine-treated I-LNC(Ox) which failed to transfer reactivity to Ox, did not interfere with the development of CS to DNFB at the same site. Finally, cotransfer experiments indicated that the effect of reserpine on the transfer of CS was not due to activation of suppressor cells. Our findings strongly suggest that whatever effects reserpine might have on immunologically nonspecific host cells, the drug's effects on sensitized T cells are sufficient to explain its ability to block cell-mediated immune responses in vivo.

Animals↗
PubMed1986

Nigral-induced decrease in striatal blood flow and the influence on this decrease of several drugs in reserpinized and non-reserpinized cats.

The effect of nigral electrical stimulation on regional blood flow in the caudate nucleus and the cerebral cortex, and the influence of several drugs on these effects were examined in reserpinized or non-reserpinized cats. A double-thermistor element was inserted into the left caudate nucleus, and a plate-type thermocouple element was put on the left cerebral cortex. The left substantia nigra was electrically stimulated for 10 sec through a concentric bipolar electrode with a diameter of 0.3 mm (30 Hz, 1 msec, 10-30 V). In non-reserpinized cats, the nigral stimulation caused a decrease in striatal blood flow, increase in cortical blood flow and rise in mean blood pressure. Hexamethonium (3 mg/kg, i.v.) blocked completely the rise in mean blood pressure following nigral stimulation, but did not affect a decrease in striatal blood flow, indicating that a decrease in striatal blood flow following nigral stimulation was not due to the activation of the peripheral sympathetic nervous system. Nigral-induced decrease in striatal blood flow in non-reserpinized cats was blocked by haloperidol (0.1 mg/kg, i.v.), methysergide (1 mg/kg, i.v.) and reserpine (2 mg/kg, i.v.), but not by phentolamine (7 mg/kg, i.v.). In reserpinized cats, nigral stimulation caused an increase in striatal blood flow in contrast to a decrease in non-reserpinized cats. After administration of 5-HTP (50 mg/kg, i.v.) in reserpinized cats, nigral stimulation decreased the striatal blood flow. On the other hand, after administration of L-DOPA (30 mg/kg, i.v.) in reserpinized cats, nigral stimulation increased striatal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Hydroxytryptophan↗
PubMed1987

Inhibition of norepinephrine transport and reserpine binding by reserpine derivatives.

Reserpine, a competitive inhibitor of catecholamine transport into adrenal medullary chromaffin vesicles, consists of a trimethoxybenzoyl group esterified to an alkaloid ring system. Reserpine inhibits norepinephrine transport with a Ki of approximately 1 nM and binds to chromaffin-vesicle membranes with a KD of about the same value. Methyl reserpate and reserpinediol, derivatives that incorporate the alkaloid ring system, also competitively inhibit norepinephrine transport into chromaffin vesicles with Ki values of 38 +/- 10 nM and 440 +/- 240 nM, respectively. Similar concentrations inhibit [3H]reserpine binding to chromaffin-vesicle membranes. 3,4,5-Trimethoxybenzyl alcohol and 3,4,5-trimethoxybenzoic acid, derivatives of the other part of the reserpine molecule, do not inhibit either norepinephrine transport or [3H]reserpine binding at concentrations up to 100 microM. Moreover, trimethoxybenzyl alcohol does not potentiate the inhibitory action of methyl reserpate. Therefore, the amine binding site of the catecholamine transporter appears to bind the alkaloid ring system of reserpine rather than the trimethoxybenzoyl moiety. The more potent inhibitors are more hydrophobic compounds, suggesting that the reserpine binding site is hydrophobic.

Adrenal Medulla↗
PubMed1997

Different concepts in first-line treatment of essential hypertension. Comparison of a low-dose reserpine-thiazide combination with nitrendipine monotherapy. German Reserpine in Hypertension Study Group.

Low-dose combination therapy has been proposed as a rational first-line approach to hypertension treatment. We compared the efficacy and tolerability of the fixed combination of reserpine (0.1 mg) plus the thiazide clopamid (5 mg) with its single components and the calcium-antagonist nitrendipine (20 mg) in a randomized, double-blind, parallel study of 273 hypertensive patients with diastolic blood pressure (BP) between 100 and 114 mm Hg. The four groups did not differ regarding baseline characteristics (mean age, 58 years; 51% men; mean BP after a 2-week placebo period, 158 to 160/103 to 104 mm Hg). After 6 weeks of treatment with one capsule daily, mean reductions in sitting BP from baseline at 24 hours after dosing in the reserpine-clopamid combination, reserpine, clopamid, and nitrendipine groups were -23.0/-17.1, -14.0/-11.7, -13.6/-11.9, and -11.6/-12.3 mm Hg, respectively (2P < .01). The corresponding normalization rates (diastolic BP < 90 mm Hg) were 55%, 40%, 36%, and 33% (2P = .11). All patients whose BP had not been normalized at this point received two capsules of the respective medication once daily from weeks 7 to 12. At week 12, mean BP reductions were -25.7/-18.1, -14.6/-12.2, -17.7/-13.4, and -14.9/-15.3 mm Hg in the four groups, respectively (2P < .01). The respective normalization rates were 69%, 35%, 39%, and 45% (2P < .0001). Linear regression modeling indicated that reserpine and clopamid combined acted more than additively. As regards tolerability, adverse experiences were observed in 27%, 28%, 29%, and 48% of patients, respectively (2P < .05). The respective rates of premature discontinuation because of adverse effects were 3%, 3%, 7%, and 13% (2P = .06). In conclusion, a low-dose combination of reserpine and clopamid lowered BP significantly more than both the components alone and nitrendipine. Moreover, the combination was tolerated as well as its components and significantly better than nitrendipine. Thus, the use of this low-dose reserpine-thiazide combination appears to be a rational alternative to conventional monotherapy in the first-line treatment of hypertension.

Adolescent↗
PubMed1983

The effect of reserpine, syrosingopine, and guanethidine on the retention of discriminated escape reversal: peripherally administered catecholamines cannot reverse the reserpine amnesia in this situation.

In a series of experiments, the effects of reserpine, syrosingopine, and guanethidine on retention of a discriminated escape reversal training were investigated in mice. The peripherally and centrally acting reserpine produced amnesia while the primarily peripherally acting compounds, syrosingopine or guanethidine, did not produce amnesia even when given in high dosages or when training was given with low footshock. Unlike in the passive avoidance situation, peripherally administered norepinephrine or dopamine was not able to attenuate the reserpine-induced amnesia. The results were discussed in terms of the role of biogenic amines in memory formation.

Animals↗
PubMed1983

Cyclic AMP phosphodiesterase activity in rat brain following chronic treatment with lithium, imipramine, reserpine, and combinations of lithium with imipramine or reserpine.

The adaptability of the cyclic AMP phosphodiesterase (PDE) following chronic treatment (4-6 weeks) with lithium, reserpine, imipramine, and combinations of lithium with imipramine or reserpine has been studied in rat brain tissue. All drugs, except lithium, were given intraperitoneally once a day. Control animals received only vehicle. Lithium was given in the diet in a concentration yielding a plasma level of 0.5-0.6 mmol/l. The PDE activity was measured in homogenates from cerebral cortex and "limbic" forebrain. These two brain areas were both found to contain three types of PDE activity. One was mainly associated with the pellet after a 10,000 X g centrifugation for 10 min. This enzyme hydrolyzed both cyclic AMP and cyclic GMP with a Km value of 130 +/- 48 microM for cyclic AMP, but was insensitive to calcium and calmodulin. Two types were mainly found in the supernatant after the centrifugation with Km values cyclic AMP of 300 +/- 108 microM and 4 +/- 3 microM, respectively. The former hydrolyzed both cyclic AMP and cyclic GMP and was stimulated 7-fold by calcium and calmodulin, while the latter only hydrolyzed cyclic AMP and was insensitive to calcium and calmodulin. None of the treatments affected the "pellet" enzyme or the low affinity enzyme from the supernatant. However, lithium treatment, even combined with reserpine or imipramine, increased the high affinity enzyme. This increase was also apparent in the DEAE-ion exchange chromatographic profile of the PDE enzymes.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

No change in rat cerebral cortex calmodulin content following chronic treatment with lithium, reserpine, imipramine, and lithium combined with reserpine or imipramine.

Rats were treated 2-3 weeks with lithium, reserpine, imipramine, and combinations of lithium with reserpine or imipramine. Lithium was given in the diet, while the other drugs were dissolved in 0.9% saline and given intraperitoneally twice daily. The control and lithium groups received only vehicle injections. Twenty-four hours after the last injection the rats were decapitated and the cerebral cortex dissected. The tissue was sliced and the noradrenaline-stimulated cyclic AMP accumulation determined or the tissue was homogenized and centrifuged at 10,000 X g for 30 min. and the calmodulin content determined in the pellet and the supernatant. Reserpine treatment was found to cause an 50% increase in the noradrenaline-stimulated cyclic AMP accumulation, while treatment with imipramine and the combination lithium-imipramine decreased the noradrenaline-stimulated cyclic AMP accumulation by 40%. The tissue content of calmodulin was, however, found unaltered by all treatments.

Animals↗
PubMedDate not supplied

Chlorthalidone plus reserpine versus hydrochlorothiazide plus reserpine in a stepped-care approach to the treatment of essential hypertension.

The efficacy of thiazide-like chlorthalidone, 50 mg, plus reserpine, 0.25 mg, was compared with that of hydrochlorothiazide, 50 mg, plus reserpine, 0.125 mg, in a six-week double-blind study of 57 patients with essential hypertension unresponsive to diet control and diuretic (step 1) therapy. An average decrease in diastolic pressure of 17.0 mm Hg was attained at the end of week 6 by the chlorthalidone/reserpine group; the average drop in the hydrochlorothiazide/reserpine group was 18.6 mm Hg. Both treatment groups displayed greater blood pressure control each week than the preceding week; and, at the end of week 6, both groups attained control of at least 5 mm Hg below the diastolic goal pressure of 90 mm Hg. The chlorthalidone/reserpine-treated group required fewer titrations than the hydrochlorothiazide/reserpine-treated group. There were no reports of frequent or severe side effects with either drug.

Adult↗