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PubMed1961

Effect of reserpine on the 5-hydroxytryptamine and adenosinetriphosphate of the dog intestinal mucosa.

Homogenates were prepared of the mucous membrane of the small intestine from dogs previously treated with high doses of reserpine. The granular material sedimented from these homogenates was centrifuged over a density gradient. The dense fraction usually rich in adenosinetriphosphate and 5-hydroxytryptamine contained little amine and no nucleotide; on the other hand, the less dense material, believed to consist mainly of mitochondria, contained amounts of adenosinetriphosphate similar to those found in animals not treated with reserpine.

Adenine Nucleotides↗

PubMed1962

Effect of chlorpromazine and reserpine on the catechol amine content of different areas of the central nervous system of the dog.

The effects of chlorpromazine and reserpine on the noradrenaline and adrenaline contents of the frontal cortex, the hypothalamus, the hippocampus and the midbrain were studied in the dog. In control dogs, the catechol amine concentrations were highest in the hypothalamus and lowest in the frontal cortex and the hippocampus. Noradrenaline contents were about seven to nine times as high as those of adrenaline in all the areas. Small doses of chlorpromazine raised the catechol amines in all the areas, the rise being maximum with 5 mg/kg. With increase in the dose of chlorpromazine there was a gradual reversal of the effect and, with 25 mg/kg, there was diminution of noradrenaline content in all the areas except in the hypothalamus. In general, chlorpromazine produced a greater rise in adrenaline than it did of noradrenaline content, and the increase of both amines was very high in the midbrain and the hippocampus compared with the other areas. Reserpine, however, depleted the catechol amine contents of all areas. The depletion was greatest for noradrenaline, an effect quite marked in the midbrain and the frontal cortex. It was concluded that the actions of these two tranquillizers on the catechol amines of dog brain differed both as to site and mechanism.

Animals↗

PubMed1962

Effects of single and repeated doses of reserpine on the secretion of adrenocorticotrophic hormone.

The effects of single and repeated doses of reserpine on the secretion of adrenocorticotrophic hormone (ACTH) were studied in rats by determining changes in the adrenal and plasma concentrations of corticosterone, in the adrenal ascorbic acid levels, and in the adrenal gland weights. Treatment with doses of reserpine which induced sedation caused prolonged hypersecretion of ACTH. Such treatment did not impair the release of ACTH in response to a stressful stimulus as recorded by an increase in the plasma corticosterone even when there was no concomitant depletion in the adrenal ascorbic acid. This finding casts doubt on the value of the adrenal ascorbic acid determination as an index of ACTH secretion.

Adrenal Glands↗

PubMed1968

Restoration of the chronotropic effect of tyramine on rat atria after reserpine.

1. The restoration by various sympathomimetic amines of the chronotropic response to tyramine was studied on the isolated atria of rats pretreated with reserpine. The atria were exposed to the "restorative" sympathomimetic amine for 10 min, washed over a period of 1 hr and then tested with 10 muM tyramine. The effect of noradrenaline, dopamine and norphenylephrine before and after inhibition of monoamine oxidase by 0.5 mM iproniazid were compared with their alpha-methyl and N-alkyl analogues in their ability to restore the chronotropic response to tyramine.2. Noradrenaline and adrenaline restored the chronotropic response to tyramine, the degree of restoration depending on the concentration of the restorative amine used. Noradrenaline after iproniazid and alpha-methylnoradrenaline were equipotent and were about 1,000 times more active than noradrenaline where monoamine oxidase was not inhibited. Dopamine, epinine, norphenylephrine, phenylephrine, octopamine, synephrine and isoprenaline in the absence of monoamine oxidase inhibition had no effect. Dopamine after iproniazid and alpha-methyldopamine were equipotent and were about 1/10 as active as alpha-methylnoradrenaline. Norphenylephrine after iproniazid and metaraminol were equipotent and were about 1/500 as active as alpha-methylnoradrenaline. Octopamine after iproniazid was even less active. The N-methylated analogues were about 1/10 as active as their nor-compounds but the N-isopropyl analogue, isoprenaline, was devoid of activity.3. Dopamine after iproniazid and alpha-methyldopamine were inactive if a dopamine-beta-hydroxylase inhibitor, disulphiram or sodium diethyldithiocarbamate, was present.4. It is concluded that, in atria of reserpinized rats, (a) protection from monoamine oxidase increases; (b) N-substitution decreases; and (c) hydroxyl groups at the beta-carbon and ring positions 3 and 4 increase the capabilities of a sympathomimetic amine to restore the chronotropic response to tyramine.

Animals↗

PubMed1971

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus).

1. The catecholamines in toad ventricle were adrenaline (90%) and noradrenaline (10%); there was no dopamine.2. Phenoxybenzamine and tyramine stimulated the isolated heart and reduced the catecholamine content.3. Reserpine treatment of toads kept at 20 degrees C did not affect the adrenaline but reduced the noradrenaline content of the ventricle.4. At 37 degrees C, reserpine caused depletion of both adrenaline and noradrenaline, and the stimulant actions of phenoxybenzamine and tyramine were lost.

Adrenergic Agents↗

PubMed1975

Tolerance to morphine-induced calcium depletion in regional brain areas: characterization with reserpine and protein synthesis inhibitors.

1 Administration of a single dose of morphine sulphate (25 mg/kg) induces tolerance to calcium depletion lasting seven days. 2 There are no apparent changes in calcium content in any of eight discrete brain regions throughout this seven day period. 3 Pretreatment with reserpine (5 mg/kg) did not alter the ability of morphine to induce tolerance. Reserpine alone produced no tolerance to its own calcium depleting action. 4 Cycloheximide (500 mug/kg) but not chloramphenicol (200 mg/kg) effectively prevented development of tolerance. 5 It is concluded that the induction of tolerance to calcium depletion seen after morphine may involve changes in various proteins in membranes of synaptic origin.

Animals↗

PubMed1975

The effect of reserpine on hypothalamo-pituitary-adrenocortical function in the rat.

1. The effect of reserpine on hypothalamo-pituitary-adrenocortical (HPA) function in the rat was investigated by the use of direct and indirect indices of pituitary adrenocorticotrophic activity. 2. Administration of a single dose of the drug induced prolonged hypersecretion of corticotrophin (ACTH). 3. Corticotrophin release in response to the drug no longer occurred after repeated daily injections, indicating that some form of 'adaptation' occurred. 4. The increase in HPA activity normally caused by exposure to cold was prevented by reserpine once 'adaptation' to the drug had been produced. 5. Inhibition of stress-induced ACTH release was due neither to depletion of pituitary stores of the hormone, nor to a corticosteroid feedback effect.

Adrenal Cortex↗

PubMed1979

Hypertension in the elderly: review of therapy with a hydroflumethiazide-reserpine combination.

A retrospective analysis revealed that 125 geriatric patients had been treated for mild to moderate essential hypertension with a combination drug, each tablet of which contained 50 mg of hydroflumethiazide and 0.125 mg of reserpine. The dosage schedule was one tablet once daily for most patients. The duration of treatment ranged from 1 to 93 months (mean, 22.1 months). After one month of therapy, the decreases in mean systolic (-18.3 mm Hg) and mean diastolic (-6.6 mm Hg) blood pressure were statistically significant and these initial reductions were well maintained over a 6-year period, without signs of tachyphylaxis. Side effects were reported by 53 patients, but these usually were mild and typical of those associated with antihypertensive therapy; discontinuation of treatment was required in only 3 patients. Use of the hydroflumethiazide-reserpine combination was associated with several significant advantages, including convenient once-daily dosing, improved compliance, and decreased cost.

Aged↗

PubMed1983

The use of reserpine for elderly hypertensive patients.

Antihypertensives are among the most commonly prescribed drugs for the elderly. Several studies have discussed the benefits of stepped-care drug therapy for hypertension in the elderly, and propranolol, methyldopa, and more recently, clonidine and prazosin have been recommended as step-two antihypertensive drugs. Recent articles omit reserpine as an alternative. A case is made for the use of reserpine by comparing factors of special importance to most elderly: cost, side-effects, frequency of dosage, number of tablets, and the effect of omitted doses.

Aged↗

PubMed1995

Antagonism of reserpine-induced suppression of spontaneous motor activity by stimulation of 5-HT1A receptors in rats.

The 5-HT1A and the DA D2 receptor agonists 8-OH-DPAT (0.05-3.2 mg kg-1 subcutaneously, -20 min.) and quinpirole (0.08-1.25 mg kg-1 subcutaneously, -20 min.), respectively, both partially antagonized reserpine-induced (5 mg kg-1 subcutaneously, -16 hr) suppression of spontaneous motor activity in the rat. Four different aspects of the spontaneous motor activity were recorded in a photocell-equipped open-field (8 x 8 photocells, 90 mm apart, defining two horizontal planes): locomotor activity (all photocell counts at the lower level); rearing (all photocell counts at the upper level); forward locomotion (the proportion movements across the arena); peripheral activity (the proportion locomotor activity as picked up by the photocell beam closest to the wall, i.e. 25 mm). As defined by these variables, the pattern of activity produced by 8-OH-DPAT or quinpirole were indistinguishable. The effects produced by 8-OH-DPAT were fully antagonized by the 5-HT1 antagonist (-) pindolol (4 mg kg-1 subcutaneously, -30 min.), but not by the DA D2 receptor antagonist raclopride (2 mg kg-1 subcutaneously, -30 min.) nor by the 5-HT2 receptor antagonist ritanserin (2 mg kg-1 subcutaneously, -30 min.), whereas effects produced by quinpirole were fully antagonized by raclopride (2 mg kg-1 subcutaneously, -30 min.). Effects produced by quinpirole, but not 8-OH-DPAT, were potentiated by administration of the DA D1 agonist SKF-38,393 (3 mg kg-1 subcutaneously, -20 min.). It is concluded that effects by 8-OH-DPAT on spontaneous motor activity in the reserpine treated rat primarily are due to stimulation of postsynaptic 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1987

L-dopa esters as potential prodrugs: effect on brain concentration of dopamine metabolites in reserpinized mice.

The intraperitoneal administration of L-dopa and a series of ester prodrugs of L-dopa to reserpinized mice produced elevations of striatal and tuberculum olfactorium homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) levels. Differences in the pattern of change produced by individual drugs, compared with L-dopa, were observed. Only the phenoxyethyl ester caused elevations of both striatal and tuberculum olfactorium HVA and DOPAC, greater than those measured following L-dopa administration. Overall the m-trifluoromethylbenzyl, phenylethyl, p-chlorophenylethyl and p-methoxyphenylethyl ester prodrugs produced greater elevations of striatal and tuberculum olfactorium HVA, but not DOPAC, compared with L-dopa. The administration of the 2-tetrahydropyranyl-methyl derivative only enhanced striatal HVA and striatal and tuberculum olfactorium DOPAC concentrations. Changes of HVA and DOPAC tissue concentrations following administration of the 2-hydroxypropyl, n-propyl, methyl, ethyl and 2-(1-methoxy)propyl ester prodrugs were comparable with those produced by the administration of L-dopa itself. The alterations in striatal and tuberculum olfactorium HVA and DOPAC levels observed did not correlate with the ability of these compounds to elicit locomotor activity in reserpinized mice.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1988

Importance of D-2 mechanisms in the reversal of reserpine hypothermia in the mouse.

The D-2 agonist LY 171555 (0.05, 0.1, 0.2 mg kg-1 s.c.) but not the D-1 agonist SK&F 38393 (5, 10, 20 mg kg-1 s.c.) reduced reserpine-induced hypothermia (RIH) in mice. This effect was antagonized by the D-2 antagonist (-)-sulpiride (50 mg kg-1 i.p.) but not by the D-1 antagonist SCH 23390 (0.1 mg kg-1 s.c.). SK&F 38393 (20 and 1 mg kg-1 s.c.) did not alter the effect of LY 171555 (0.1 and 0.2 mg kg-1) on RIH, but administration of both LY 171555 (0.2 mg kg-1 s.c.) and SK&F 38393 (1 mg kg-1 s.c.) antagonized the reserpine-induced sedation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1993

Stimulation of brain dopamine autoreceptors by remoxipride administration in reserpine-treated male rats.

Male Sprague-Dawley rats were treated subcutaneously with reserpine (5 mg kg-1, -18 h) and with the aromatic amino acid decarboxylase inhibitor, NSD-1015 (3-hydroxybenzylhydrazine) (100 mg kg-1 -30 min). Remoxipride 0.8, 3.2 or 12.8 mg kg-1 was administered subcutaneously at -50 min. Immediately following decapitation (0 h), the ventral striatum and the anterior neocortex were dissected. Dopa and 5-hydroxytryptophan accumulation in these brain areas were analysed by HPLC with electrochemical detection. Reserpine produced a marked increase in striatal and neocortical dopa accumulation, in comparison with glucose vehicle + NSD-1015-treated controls, and this increase was dose-dependently antagonized by remoxipride treatment. Thus, together with demonstrated dopamine receptor antagonist actions in intact animals, remoxipride behaves as a mixed dopamine receptor agonist-antagonist. Such properties could contribute to the favourable endocrine and extrapyramidal side effect profile of remoxipride as an antipsychotic agent.

5-Hydroxytryptophan↗

PubMed1960

Effect of reserpine on ventricular escape.

Catecholamine depletion by reserpine diminishes the tendency of the ventricle to escape from vagal suppression. Neither spinal section nor adrenalectomy enhances the reserpine effect. Norepinephrine restores the characteristic occurrence of ventricle escape during vagal stimulation.

Catecholamines↗

PubMed1978

Calcium influx and spontaneous phasic contractions of portal veins after treatment with reserpine, 6-hydroxydopamine, and cocaine.

Reserpine treatment increased the amplitude of the spontaneous phasic contraction (SPC) of portal veins obtained from rabbit and guinea pig but did not alter that of rat. The amplitude of the SPC of portal veins from these animals was increased after 6-hydroxydopamine (6-OHDA) but was not changed after cocaine treatment. Reserpine- and 6-OHDA-induced changes in portal vein SPC amplitude were accompanied by an increase in 45Ca influx. These results indicate that the elevation in SPC amplitude is accompanied by an increase in calcium influx.

Animals↗

PubMed1978

Protection by zinc sulphate against reserpine-induced ulceration and other gastric effects in the rat.

The effects of intraperitoneal pretreatment, 48 h beforehand, with zinc sulphate (22, 44 or 88 mg/kg) were studied on gastric ulceration, gastric secretion and changes in stomach wall mast cell counts induced after 4 h by reserpine (5 mg/kg) given intraperitoneally to intact (unoperated for pylorus occlusion) or pylorus-occluded rats. Zinc sulphate dose-dependently antagonised the gastric actions of reserpine by preventing ulceration in the ruminal and glandular segments of the stomach, reducing acid secretion, and inhibiting mast cell degranulation which occurred mainly in the glandular mucosal layer. The relationship between these findings and the action of zinc on gastric mast cell is discussed.

Animals↗

PubMed1981

Effects of alpha-methylnoradrenaline and alpha-methyldopamine in reserpine-induced ulcers in rats.

alpha-Methyldopamine and alpha-methylnoradrenaline administered intraperitoneally afforded significant protection in reserpine-induced ulcers in rats. The optimal doses were 2 and 4 mg/kg. Lower and higher doses were less effective. alpha-Methyldopamine and alpha-methyl-noradrenaline probably act by reestablishing the normal adrenergic tone which is diminished in reserpine-induced ulcers.

Animals↗

PubMed1985

Effect of postganglionic denervation and pretreatment with reserpine on alpha-adrenoceptors of the guinea-pig vas deferens.

The radiolabeled alpha-1-adrenoceptor antagonist [3H]WB-4101 was used to determine whether supersensitivity of the guinea pig vas deferens that develops after denervation or reserpine pretreatment is associated with a change in the characteristics of the alpha-1-adrenoceptor. Specific binding of [3H]WB-4101 to membrane fractions of vasa deferentia was saturable and reversible. The dissociation constant (KD) was similar when obtained by equilibrium or kinetic studies. As determined by Scatchard analysis, neither chronic (5 days) pretreatment with reserpine (1.0 mg/kg/day) nor postganglionic denervation (7 days) altered the number or affinity of [3H] WB-4101 binding sites. It is concluded that changes in alpha-1-receptor characteristics are not responsible for postjunctional supersensitivity in this tissue.

Adrenergic alpha-Antagonists↗