Central nervous system effects of four β-adrenergic receptor blocking agents

Murmann, W; Almirante, L; Saccani-Guelfi, M

doi:10.1111/j.2042-7158.1966.tb07878.x

Cited by 128 publications

(27 citation statements)

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“…These findings indicate that the anti-tremor actions of propranolol are not due to the blockade of the adrenergic P-receptors but may be due to other pharmacological actions. Propranolol has been reported to produce depression of the central nervous system (Murmann, Almirante & Saccani-Guelfi, 1966) and shows central muscle relaxant effects (Sinha, Srimal, Jaju & Bhargava, 1966). These effects may be responsible for its anti-tremor action.…”

Section: Discussionmentioning

confidence: 99%

A Study of the Role of Brain Catecholamines in Drug Induced Tremor

Agarwal

Böse

1967

British Journal of Pharmacology and Chemotherapy

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In a recent study, Owen & Marsden (1965) have shown that adrenaline increases and that the adrenergic ft-receptor blocking drugs, pronethalol and propranolol, diminish tremor in patients with Parkinson's disease. Vas (1966), however, did not observe any effect of propranolol in Parkinsonian tremor.Friedman (1963) andFriedman, Aylesworth &Friedman (1963) have shown that tremorine lowers the noradrenaline levels in the brains of rats, mice and guinea-pigs but fails to do so in rabbits, which do not show tremor after the administration of tremorine.These findings indicate that brain catecholamines may have a role in causing tremor and the present work was undertaken to study their role in, and the effect of, a recent adrenergic f,-receptor blocking drug-namely, dextro-N-isopropyl-para-nitrophenylethanolamine (d-INPEA)-on tremorine and harmaline induced tremor in mice. METHODSTremor was recorded by a modification of the method of Ahmed & Taylor (1959). A perforated plastic box 5 in x 3 in x 2 in was bolted to a 31 in brass rod (* in diameter), which in turn was fixed into the position of the stylus of a high impedance (6,000Q) electromagnetic gramophone pick-up. Lateral movements of the box were converted by the pick-up into electrical changes, which were amplified and recorded on one channel of a Grass four channel electroencephalograph. The amplification level was kept at a minimum. The paper speed was 15 mm/sec. The whole device was kept in a sound-proof booth. Sixty male mice, weighing between 22-27 g, fed in the morning on the day of experiment, were used. They were placed in the box, one at a time, for 10-15 min before each experiment, in order to acclimatize them. This ensured a very low baseline due to reduced spontaneous activity of the mice. After a control period, one of the two tremorogenic drugs was injected intraperitoneally (tremorine 20 mg/kg and harmaline 30 mg/kg) and movements were recorded every 5 min for 60 min. After establishing that in the doses given, all the mice showed tremor after the drugs, they were divided into six groups of 10 mice.The mice in each group received one of the drugs used in the present study, intraperitoneally, and each group then was further divided into two subgroups of five animals each, for challenging with tremorine and harmaline. The effects of these tremorogenic drugs were then followed for a period of 1 hr.The various drugs used for modifying tremor were: reserpine (Serpasil; Ciba), alpha-methylmeta-tyrosine (Merck, Sharp and Dohme), pargyline (Abbot), propranolol (I.C.I.), d-INPEA and I-INPEA (Selvi).

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Section: Discussionmentioning

confidence: 99%

A Study of the Role of Brain Catecholamines in Drug Induced Tremor

Agarwal

Böse

1967

British Journal of Pharmacology and Chemotherapy

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“…PROP has a CNS depressive effect such as an anticonvulsive effect, suppression of fighting behavior and enhancement of sleeping time induced by hexobarbiton (20,21). These effects have been suggested to be unrelated to the beta-receptor blockade (20,21). These depressive effects also resemble the central action of benzodiaze pines like CDP.…”

Section: Discussionmentioning

confidence: 87%

“…Beta-antagonists possess several phar macological actions such as beta-receptor blockade, membrane stabilizing effect, intrinsic sympathomimetic activity, and de pressive effect on the central nervous system (CNS). PROP has a CNS depressive effect such as an anticonvulsive effect, suppression of fighting behavior and enhancement of sleeping time induced by hexobarbiton (20,21). These effects have been suggested to be unrelated to the beta-receptor blockade (20,21).…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Haloperidol-induced Catalepsy by Beta-Adrenoceptor Antagonists in Mice

Hara

Ogawa

1986

Japanese Journal of Pharmacology

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Abstract-Severalclinical papers have reported that beta-adrenoceptor antagonists were useful in the management of schizophrenia and tardive dyskinesia. The present study examined effects of beta-antagonists on haloperidol (HAL)-induced catalepsy using mice in order to study the relationship between beta-antagonists and central dopaminergic functions. Catalepsy was tested by the standard bar test 30 min after intraperitoneal treatment of HAL. Beta-antagonists were admin istered subcutaneously just after HAL-treatment. Propranolol, alprenolol, oxprenolol and pindolol increased the incidence of catalepsy compared to HAL alone. Atenolol, not penetrating into the brain, and the sedative and hypnotic drug chlord 1azepoxide did not potentiate it. These results suggest that the potentiation of HAL-catalepsy by beta-antagonists is based on their central action. Therefore, a central beta receptor appears to be implicated in the regulation of the central dopaminergic functions.

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“…It is interesting that some of these drugs have been reported to interfere with normal sleep/wakefulness patterns (Bradley & Elkes, 1957;Bradley & Hance, 1957;Murman, Almirante & Saccani-Guelfi, 1966). Such effects could be, in part, the result of an action within the raphe system, whereby the level of tonic noradrenergic inhibitory influences are altered and thus the balance between sleep and wakefulness disturbed.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Electrocortical Changes Induced by (+)‐amphetamine and Chlorpromazine When Perfused Directly Into the Dorsal Raphe Nucleus of the Cat

Key¹,

Krzywosiński²

1978

British J Pharmacology

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1 (+ )-Amphetamine mimicked the intermittent and sustained electrocortical desynchronization produced by (-)-noradrenaline (NA) when perfused directly into the dorsal raphe nucleus of cat encephale isole preparations. 2 The effects of amphetamine or NA were abolished or significantly attenuated by prior application of (-)-propranolol. 3 The effect of amphetamine, but not that of NA, was blocked by prior applications of guanethidine or chlorpromazine (CPZ). 4 Desmethylimipramine (DMI) produced dose-related changes in electrocortical activity which were similar to those induced by NA when applied to the same sites within the dorsal raphe nucleus. 5 DMI potentiated the effects of both amphetamine and NA, but guanethidine only abolished the DMI-induced potentiation of the amphetamine response. 6 (-)-Propranolol, guanethidine and CPZ produced a short period of electrocortical desynchronization at the beginning of the perfusion period before antagonism of the amphetamine response was apparent.7 The results suggest that CPZ and amphetamine have an action within the dorsal raphe nucleus possibly related to noradrenergic terminals.

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Central nervous system effects of four β-adrenergic receptor blocking agents

Cited by 128 publications

References 1 publication

A Study of the Role of Brain Catecholamines in Drug Induced Tremor

A Study of the Role of Brain Catecholamines in Drug Induced Tremor

Potentiation of Haloperidol-induced Catalepsy by Beta-Adrenoceptor Antagonists in Mice

Comparison of the Electrocortical Changes Induced by (+)‐amphetamine and Chlorpromazine When Perfused Directly Into the Dorsal Raphe Nucleus of the Cat

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