Adrenergic control of tendon jerk reflexes in man

Phillips, Sandra J.; Richens, A.; Shand, David G.

doi:10.1111/j.1476-5381.1973.tb08190.x

Cited by 24 publications

(18 citation statements)

References 13 publications

(16 reference statements)

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“…Comparison with previously published results (Phillips et al, 1973) suggests that thymoxamine was more potent than chlorpromazine in depressing the triceps surae jerk, and three times as potent as indoramin. Isolated tissue experiments have shown consistently that thymoxamine is a weaker ax-adrenoceptor blocker than chlorpromazine or indoramin (Birmingham & Szolcsanyi, 1965;Collis & Alps, 1973;Gorlitz & Frey, 1973;Variava & Turner, 1973;Sugden, 1974).…”

Section: Discussionmentioning

confidence: 72%

“…The amplitude of the triceps surae jerk was measured isometrically using the method previously described by Phillips et al (1973), modified to the extent that the subjects were lying instead of sitting. A standard tap was delivered to the Achilles tendon by a hammer dropped from a fixed height.…”

Section: Methodsmentioning

confidence: 99%

“…Phillips, Richens & Shand (1973) showed that intravenously administered thymoxamine had a marked depressant effect on the triceps surae (ankle) jerk in normal human subjects, while propranolol produced no change in jerk size. Thymoxamine did not appear to affect maximal H reflex responses, and it was concluded that it could be acting by blockade of facilitatory pathways controlling fusimotor activity.…”

Section: Introductionmentioning

confidence: 99%

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Α‐adrenoceptor Blocking Drugs, Pressor Responses to Noradrenaline, and the Ankle Jerk in Man

White

Richens

1974

Brit J Clinical Pharma

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Changes in pressor responses to infused noradrenaline and in triceps surae jerk amplitude have been measured after the i.v. administration of: chlorpromazine, thioridazine, prochlorperazine, dimethothiazine, indoramin, benzoctamine and clonidine. Each of the drugs blocked pressor responses to noradrenaline and reduced triceps surae jerk amplitude, but little correlation was found between their potencies in the two systems. The effects of the drugs on the triceps surae jerk are not incompatible with an action at a spinal α‐adrenoceptor site, but other pharmacological factors may be involved, such as penetration of the drugs into the central nervous system, and differences in their uptake1 blocking activity.

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Section: Discussionmentioning

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Α‐adrenoceptor Blocking Drugs, Pressor Responses to Noradrenaline, and the Ankle Jerk in Man

White

Richens

1974

Brit J Clinical Pharma

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“…Since blockade of peripheral a-adrenoceptors would account for the reduced hypertensive response but not the reduced bradycardia (which was mediated by increased cardiac vagal tone) it is possible that thymoxamine antagonized a-adrenoceptors in the anterior hypothalamus. Since thymoxamine readily penetrates the CNS (Pruvot, Agneray & Hdquet, 1969;Phillips, Richens & Shand, 1973), it was not possible to determine the contribution made by increased sympathetic drive to noradrenaline-induced hypertension.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular responses of rats to intrahypothalamic injection of carbachol and noradrenaline

Poole

1983

British J Pharmacology

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Carbachol (0.1–2 μg) and noradrenaline (5–20 μg) injected into the anterior hypothalamus of unanaesthetized unrestrained rats evoked dose‐dependent falls in heart rate and increases in arterial blood pressure. When the above amine injections were repeated in rats anaesthetized with chloral hydrate, sodium pentobarbitone or halothane the evoked bradycardias were usually smaller and the changes in arterial blood pressure more variable. The cardiovascular responses to carbachol (1 μg) and to noradrenaline (10 μg) were antagonized by intrahypothalamic injection of atropine (1 μg) and phentolamine (10 μg), respectively. The bradycardias evoked by carbachol (1 μg) and by noradrenaline (10 μg) were abolished by pretreatment with intra‐arterial injection of methyl atropine (100 μg 100 g−1). The hypertensive responses to carbachol (1 μg) and to noradrenaline (10 μg) were reduced by pretreatment with intra‐arterial injection of thymoxamine (500 μg 100 g−1).

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“…Descending adrenergic pathways have been described (Dahlstrbm & Fuxe, 1965;Fuxe, H6kfelt & Ungerstedt, 1969), and Ellaway & Pascoe (1968) have suggested that noradrenaline may be an excitatory transmitter involved in the control of fusimotor activity. An adrenergic control of tendon jerk reflexes in man has also been suggested (Phillips, Richens & Shand, 1973).…”

Section: Experiments In the Dogmentioning

confidence: 99%

PHARMACOLOGY OF M & B 18,706, A DRUG WHICH SELECTIVELY REDUCES DECEREBRATE RIGIDITY

Maxwell

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Sumpter

1974

British J Pharmacology

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(±)‐10‐(3‐Dimethylamino‐2‐methylpropyl)‐2‐valeroylphenothiazine hydrochloride (M & B 18,706) has been compared with dimethothiazine, chlorpromazine, diazepam and baclofen for potency in reducing decerebrate rigidity in the cat and rat and for activity in causing ataxia or sedation. When given intravenously M & B 18,706 had seven times the potency of dimethothiazine and one‐half the potency of chlorpromazine in reducing the rigidity of the intercollicular decerebrate cat. When administered orally M & B 18,706 and chlorpromazine were equi‐potent in reducing rigidity but M & B 18,706 was less effective than chlorpromazine in producing ataxia in this species. In the rat, M & B 18,706 had one‐quarter the potency of chlorpromazine for reducing decerebrate rigidity but had from 1/20th to 1/200th its potency in tests for sedative or tranquillizing activity. M & B 18,706, like dimethothiazine and chlorpromazine, had little effect on the rigidity of ischaemic decerebrate cats and failed to inhibit polysynaptic spinal reflexes. M & B 18,706 had intravenous potency comparable to chlorpromazine in reducing the pressor action of noradrenaline in the spinal cat.

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Adrenergic control of tendon jerk reflexes in man

Cited by 24 publications

References 13 publications

Α‐adrenoceptor Blocking Drugs, Pressor Responses to Noradrenaline, and the Ankle Jerk in Man

Α‐adrenoceptor Blocking Drugs, Pressor Responses to Noradrenaline, and the Ankle Jerk in Man

Cardiovascular responses of rats to intrahypothalamic injection of carbachol and noradrenaline

PHARMACOLOGY OF M & B 18,706, A DRUG WHICH SELECTIVELY REDUCES DECEREBRATE RIGIDITY

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