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PubMed1970

The effect of reserpine on the pressor responses to angiotensin in the conscious cat.

1. Blood pressure recordings have been made in conscious cats in an attempt to reveal a possible indirect component to the angiotensin pressor response.2. Reserpine (50 to 250 mug/kg per day) caused a maximal reduction of about 50% in the pressor response to angiotensin whilst virtually abolishing the responses to tyramine and McN-A-343. Responses to noradrenaline were only slightly and transiently reduced.3. Syrosingopine (0.5 mg/kg) and reserpine (250 mug/kg) reduced the responses to angiotensin, McN-A-343 and tyramine to much the same extent, but tetrabenazine only reduced the responses to all these agents in a dose (25 mg/kg) which probably had effects on the catecholamine stores of smooth muscle.4. The reduction in the responses to angiotensin, tyramine and McN-A-343 by reserpine was partly reversed by tranylcypromine. Noradrenaline and (+/-)-dopa infusions were ineffective by themselves, but increased the effects of tranylcypromine in restoring the responses to angiotensin, tyramine and McN-A-343 after reserpine.5. Infusion of alpha-methyldopa markedly increased the responses to angiotensin, tyramine and McN-A-343 after these had been reduced by reserpine.6. The results suggest that the pressor response to angiotensin in the conscious cat is partly mediated by release of noradrenaline from peripheral neuronal stores.

Angiotensin II↗

PubMed1971

Action of 6-hydroxydopamine on lamb sympathetic ganglia, vas deferens and adrenal medulla: a combined histochemical, ultrastructural and biochemical comparison with the effects of reserpine.

1. The effects of a single dose of 6-hydroxydopamine (6-OHDA) compared with those of chronic reserpine treatment were studied in lamb sympathetic neurones and adrenal medulla by a combination of fluorescence histochemistry, electron microscopy and radiochemical assay.2. In sympathetic ganglia, 6-OHDA produced a rise in noradrenaline concentration within 24 h, and falls in tyrosine hydroxylase and monoamine oxidase activities, whereas reserpine caused a fall in noradrenaline, a rise in tyrosine hydroxylase activity and no change in monoamine oxidase activity. The fluorescence of intra- and postganglionic axons increased greatly within 24 h of 6-OHDA, and there was a corresponding accumulation of large dense-core vesicles within many axons whose neurotubules were disrupted. The changes were almost reversed after 3 weeks.3. In the vas deferens, the concentration of noradrenaline and tyrosine hydroxylase and monoamine oxidase activities had all fallen 24 h after 6-OHDA treatment and had started to recover 3 weeks later. In the adrenal medulla, 6-OHDA did not alter NA concentrations but increased tyrosine hydroxylase activity whereas reserpine depleted noradrenaline and increased tyrosine hydroxylase activity.4. The changes produced in sympathetic ganglia by 6-OHDA may be due both to a direct action on the axoplasmic transport of noradrenaline containing vesicles and indirectly to the reaction of the neurones to loss of the integrity of their axons.

Adrenal Medulla↗

PubMed1973

Decreased synthesis of DNA in regenerating rat liver after the administration of reserpine.

1. Reserpine given to rats before the enhanced synthesis of DNA begins 14h after partial hepatectomy markedly depresses thymidine uptake into DNA at 24 hours.2. At this time decreased activity of liver thymidine kinase but unchanged thymidine 5'-nucleotidase were observed.3. Reserpine has no effect on DNA synthesis when administered simultaneously with the labelled thymidine 2 h before killing.4. With depressed DNA synthesis after reserpine administration there is no significant decrease of liver RNA synthesis.

Animals↗

PubMed1989

An in vivo dialysis and behavioural study of the release of 5-HT by p-chloroamphetamine in reserpine-treated rats.

1. Reserpine (2.5 mg kg-1 i.p.) decreased rat brain 5-hydroxytryptamine (5-HT) by 86% 24 h later but most components of the 5-HT-dependent behavioural syndrome induced by p-chloroamphetamine (PCA, 5 mg kg-1 i.p.) or 5-methoxy-N,N-dimethyltryptamine (5-MeODMT, 5 mg kg-1 i.p.) over 1 h after administration were unaffected. However, Straub tail was increased after giving PCA or 5-MeODMT and head weaving was decreased after giving 5-MeODMT. 2. Frontal cortex extracellular 5-HT concentrations of vehicle pretreated rats before injection of PCA, as calculated from dialysate 5-HT concentrations, were about 1/1000th of corresponding brain values. Extracellular 5-hydroxyindoleacetic acid (5-HIAA) and brain values were comparable with each other. Dialysate 5-HT increased after PCA with peak values at 20-40 min. 3. Reserpine pretreatment reduced dialysate 5-HT concentration before PCA was given but the net increase (AUC) over the 1 h after PCA did not differ significantly from that seen in animals pretreated with vehicle. Dialysate 5-HIAA values slowly decreased after PCA injection in both reserpine and vehicle pretreated groups. 4. The results suggest that PCA causes the 5-HT syndrome by releasing 5-HT from the neuronal cytoplasm but that physiological release of 5-HT occurs from vesicular stores.

Amphetamines↗

PubMedDate not supplied

Effect of nicotine and alcohol pretreatment on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats.

The effect of nicotine and alcohol pretreatment by feeding nicotine (2.5 mg/100 ml), alcohol (25%, v/v) and their combination (nicotine 2.5 mg/100 ml + alcohol 25%, v/v) in drinking water ad libitum for 21 days was studied on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats. When given alone, neither nicotine nor alcohol produced any visibly discernible gastric lesions. Their concurrent administration, however, produced minor injury to the gastric mucosa appearing as 5-7 circular ulcers of less than 1 mm in diameter. Pretreatment with nicotine, alcohol, and their combination resulted in the significant augmentation of gastric ulcers produced by aspirin, phenylbutazone, and reserpine. The augmentation of gastric lesions in the group pretreated with the combination of nicotine and alcohol was significantly greater than in the groups treated by either of them alone. The effect of nicotine on the mucus neck cell population of the gastric mucosa and pancreatic bicarbonate secretion, and the gastric mucosal damaging effect of chronic alcohol treatment may be responsible for the potentiation of ulcerogenic effects of aspirin, phenylbutazone, and reserpine.

Animals↗

PubMed1979

Inhibition of 3H-dopamine accumulation in reserpinized and normal rat striatum.

The inhibitory potencies of 27 compounds on the accumulation of 3H-dopamine (DA) in synaptosome-rich striatal homogenates of normal and reserpinized rats were determined. It was found that some compounds, e.g. amphetamine derivatives, phenmetrazine, phenethylamine derivatives and tryptamine derivatives were considerably more potent in the reserpinized preparation than in the normal one. Other compounds, e.g. amfonelic acid, mazindol, EXP 561, benztropine, pipradrol, nomifensine, methylphenidate and cocaine had similar potencies in the two preparations. It is suggested that the compounds enhanced by reserpine are more potent as DA releasing agents than as inhibitors of the DA uptake, whereas the compounds in the other group are most potent as uptake inhibitors. Interestingly, these two groups completely agree with the two groups of central stimulatory agents, viz. the amphetamine-like and the methylphenidate-like drugs.

Amphetamines↗

PubMed1980

Antagonism of reserpine-induced hypothermia in mice by some beta-adrenoceptor agonists.

The reversal of reserpine-induced hypothermia in mice be three beta-adrenoceptor agonists, terbutaline, salbutamol and clenbuterol, was examined. Terbutaline, 5 and 20 mg/kg intraperitoneally, caused a slight reversal of the hypothermia. Salbutamol, 5 mg/kg intraperitoneally, produced a pronounced and 1 mg/kg a slight reversal. Clenbuterol was very potent in reversing the hypothermic effect of reserpine with significant effect at 0.02 mg/kg intraperitoneally. Propranolol, 2.5 mg/kg intraperitoneally, and the selective beta 2-receptor antagonist IPS 339, 5 mg/kg intraperitoneally, almost completely antagonized the effect of clenbuterol, 1 mg/kg intraperitoneally. The beta-receptor antagonist metoprolol at 5 and 25 mg/kg intraperitoneally only partially antagonized the effect of clenbuterol. Since clenbuterol is much more lipophilic than salbutamol and terbutaline, it is suggested that the reserpine reversal produced by clenbuterol is at least partially of central origin and possibly mediated by stimulation of noradrenergic beta 2-receptors.

Adrenergic beta-Agonists↗

PubMed1992

Evaluation of captopril versus reserpine and frusemide in treating hypertensive children with acute post-streptococcal glomerulonephritis.

We have evaluated the effect of oral captopril versus a combination of oral reserpine and frusemide in the treatment of 20 children with post-streptococcal glomerulonephritis (APGN) with hypertension. Captopril produced a significantly greater reduction in systolic and diastolic blood pressure in both the standing and supine positions than reserpine + frusemide at 0.75, 1, 1.25, 8, 24, 48 and 72 h after initiating treatment. Neither postural hypotension nor reflex tachycardia accompanied the therapeutic effect of captopril. Blood urea, serum creatinine and creatinine clearance did not change significantly after therapy in either study group. Three days after initiating treatment, the 24 h urinary catecholamine output increased significantly in children who received captopril but did not change in children treated with frusemide and reserpine.

Acute Disease↗

PubMed1975

The role of dopamine and noradrenaline in temperature control of normal and reserpine-pretreated mice.

Drugs with the common property of stimulating dopamine receptors, have been tested for their effects on core temperature in control and reserpine-pretreated mice. Apomorphine, amantadine, amphetamine, L-dopa and atropine all produced a fall in mouse oesophageal temperature, their efficacy correlating with their ability to activate central dopamine receptors. Amphetamine and L-dopa had a biphasic effect the initial fall being followed by a rise. In reserpine-pretreated mice only amphetamine, apomorphine, L-dopa and D.L-threo-dihydroxyphenyl-serine effectively reversed hypothermia. Amphetamine had the highest efficacy of all the drugs tested. The sum of the effects of apomorphine and D.L-threo-dihydroxyphenylserine was equivalent to the effect of amphetamine alone. It is suggested that in control mice dopaminergic mechanisms mediate the hypothermia and noradrenergic mechanisms the hyperthermia. In reserpine-pretreated mice both systems are involved in the mechanisms restoring body temperature to normal.

Amantadine↗

PubMed1990

Desipramine and nortriptyline antagonize apomorphine and reserpine hypothermia by a different mechanism.

The reversal of hypothermia, induced by reserpine or by a high (16 mg) dose of apomorphine, in male Swiss mice, does not seem to utilize a common mechanism. Desipramine (20 mg kg-1 i.p., 60 min) or nortriptyline (8 mg kg-1 i.p., 60 min) increased temperature in both reserpine (2.5 mg kg-1 s.c., 18-19 h) and apomorphine (16 mg kg-1 s.c., 30 min) treated mice. In apomorphine-treated animals the effect of both drugs was reversed by the mixed dopaminergic D1- D2-antagonist haloperidol (1 mg kg-1 i.p., 90 min), the D1-receptor blocking drug SCH 23390 (0.05 mg kg-1 s.c., 30 min), the alpha 1-adrenoceptor blocking drugs prazosin (3 mg kg-1 s.c., 90 min) and phenoxybenzamine (20 mg kg-1 i.p., 65 min), the beta-adrenoceptor blocking drug (+/-)-propranolol (10 mg kg-1 i.p., 120 min), and the opioid antagonist naloxone (2 mg kg-1 i.p., 15 min). In contrast the selective D2-antagonist (+/-)-sulpiride (100 mg kg-1 i.p., 90 min), and the alpha 2-antagonist yohimbine (2 mg kg-1 i.p., 75 min), failed to effect the reversal of apomorphine hypothermia brought about by desipramine or nortriptyline. Their temperature effects in reserpinized mice were not modified by any of the antagonists tested.

Animals↗

PubMed1960

Is reserpine tranquilization linked to change in brain serotonin or brain norepinephrine?

Reserpine, when administered to animals stressed by exposure to cold, does not induce sedation or appreciably lower brain serotonin, but markedly lowers brain norepinephrine. Reserpine in cold-exposed hypophysectomized rats elicits sedation and releases both amines equally. The results support the view that the tranquilizing action of reserpine is not related to brain norepinephrine loss but rather to change in the level of brain serotonin.

Animals↗

PubMed1966

Reserpine: inhibition of olfactory blockage of pregnancy in mice.

Failure of pregnancy in newly mated female mice exposed to fresh urine from alien males is prevented by administration of reserpine, at 6.25 micrograms per day per female, on days 1 to 5 post coitum-that is, throughout the period of exposure to male urine and for 2 more days. Since reserpine is known to suppress the inhibitory center in the hypothalamus controlling the release of prolactin, inhibition by reserpine of the blockage of pregnancy provides a strong direct indication of hypothalamic mediation in the male-induced failure of pregnancy in mice.

Animals↗

PubMed1986

Is reserpine a human teratogen?

A single stillborn female with craniofacial, abdominal, and central nervous system malformations was exposed to reserpine during the first six weeks of gestation. Parallels between the malformations present in this infant and those induced in rats through exposure to reserpine at analogous periods of gestation suggest that reserpine may pose specific risks for malformations in some pregnancies.

Abnormalities, Drug-Induced↗

PubMed1976

Unmasking of sympathetic vasoconstruction of the coronary vessels after acute administration of reserpine to dogs.

Acute intravenous administration of reserpine or pretreatment of dogs with Segontin selectively abolished coronary vasodilation and unmasked a constrictor response to stimulation of the cardiac sympathetics. In view of earlier findings of separate coronary vasomotor and cardiostimulatory sympathetic innervation, the results are interpreted to indicate the existence of reserpine-resistant short (vasomotor) and reserpine-sensitive long (cardiostimulatory) sympathetic postganglionic neurons.

Animals↗

PubMed1976

Effects of reserpine on tissue calcium and contractility of rat and rabbit aorta.

Possible effects of reserpine on disposition and availability of tissue calcium, stores for excitation-contraction coupling in isolated rat and rabbit aortae were examined. Contral 40Ca uptake, 45Ca washout, and contraction in Ca2+-free medium (Ca2+-free PSS) indicate species differences in binding or disposition, apparent functional importance, and differential use of tissue calcium by adrenaline (Epi) and high K+. Rat aortae, normally refractory to Epi or high K+ after 7 min in Ca2+-free PSS, can gain labile calcium after brief exposure to Ca2+-rich PSS which supports short-lived responses to high K+ in Ca2+-free PSS. Rabbit aortae contain calcium stores which may sustain either Epi or high-K+ responses as well as more tightly held (or sequestered) stores released by Epi for contraction. After reserpine, decreased 45Ca uptake in a kinetically defined "fast" compartment likely to include membrane calcium could enhance availability of bound tissue as well as free Ca2+ in both species. Enhanced Epi response in Ca2+-free PSS is evidence of the former. Results suggest that increased availability of bound and possibly free calcium contribute to reserpine-induced supersensitivity, but supporting evidence will be required from tissue behavior after less rigorous treatment.

Animals↗

PubMed1977

Effects of reserpine on water, cation, and norepinephrine contents of cardiovascular tissues of normotensive dogs.

Six adult male mongrel dogs were treated orally with reserpine (0.03 mg/kg) for 6 weeks, after which time the arterial tissue content of water, cations (sodium, potassium, magnesium, and calcium), and norepinephrine was determined and compared with those of six untreated dogs. Reserpine administration resulted in sustained decreases in the mean arterial blood pressure and heart rate, and the arterial tissues of the treated dogs contained less potassium, calcium, and magnesium, the last-named being affected most, but the sodium remained the same. Arterial norepinephrine content was significantly decreased. There was a slight but significant increase in plasma magnesium, without any noticeable changes in other plasma cations. The reduction in the arterial magnesium by reserpine may help to regulate vascular tone and (or) vascular reactivity.

Animals↗

PubMed1977

Reserpine-induced supersensitivity to the activation of cardiac glycogen phosphorylase by calcium.

Rats receiving reserpine (2.5 mg/kg, 24 h before sacrifice) developed a supersensitivity to the phosphorylase activating effect of both noradrenaline and Ca2+. Supersensitivity to the inotropic and chronotropic effects of the agonists did not develop with this dose of reserpine. It is concluded that reserpine induced supersensitivity, as well as being dose and species dependent, is also dependent on the response measured. It is concluded further that the supersensitivity developed to noradrenaline may be due to an alteration in the responding system (in this case the phosphorylase activating system) to calcium.

Animals↗

PubMed1988

Biphasic changes in anterior pituitary Met-enkephalin concentration following reserpine treatment.

Met-enkephalin concentrations in the anterior pituitary gland were shown to decline dramatically within the first 24 h after reserpine treatment, with effects apparent as early as 6 h. This was followed by subsequent repletion and late augmentation of Met-enkephalin levels 3 weeks following reserpine. Treatment with the alpha-1-adrenergic agonist methoxamine had no effect, whereas the alpha-1-antagonist prazosin lowered Met-enkephalin concentrations. Treatment with the dopamine agonists bromocriptine or apomorphine had no effect, but haloperidol treatment increased anterior pituitary Met-enkephalin which was reversed by concomitant bromocriptine administration. We postulate that the changes in anterior pituitary Met-enkephalin following reserpine were related to alterations in the monoamine neurotransmitters. Adrenergic and dopaminergic mechanisms may have opposing roles in the maintenance of Met-enkephalin concentrations in the anterior pituitary gland.

Animals↗