Peripheral Noradrenaline and Adrenergic Transmission in the Rat

Spriggs, T. L. B.

doi:10.1111/j.1476-5381.1966.tb01830.x

Cited by 24 publications

(24 citation statements)

References 24 publications

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“…The pressor response to McN-A-343 is transient, well-defined and reproducible and is uncomplicated by the anticholinesterase disturbances associated with physostigmine. Doses of adrenergic neurone blocking agents found to block the pressor response of McN-A-343 were of the same order as those necessary to block contraction of the inferior eyelid of the rat in response to preganglionic stimulation of the ipsilateral cervical sympathetic chain (Spriggs 1966) and to depress adrenergic nerve function in other species (Boura & Green, 1965). Guanethidine was the most persistent of these drugs and the blockade by bethanidine and bretylium was of much shorter duration in rats than in cats and dogs.…”

Section: Effects On Noradrenalinementioning

confidence: 95%

“…McN-A-343 is a selective sympathetic ganglion stimulant in cats and dogs, and its pressor effects, which are attributed to increased peripheral adrenergic discharge, are blocked by bretylium (Roszkowski, 1961). The pressor action is unusual in that it is blocked by atropine but not by hexamethonium (Roszkowski, 1961 Cass & Spriggs, 1961;Varagic & Vojvodic, 1962;Gokhale et al, 1963;Spriggs, 1966). The pressor response to McN-A-343 is transient, well-defined and reproducible and is uncomplicated by the anticholinesterase disturbances associated with physostigmine.…”

Section: Effects On Noradrenalinementioning

confidence: 99%

“…A number of workers have studied the antagonism by these drugs of the increased peripheral adrenergic discharge brought about by a postulated central action of physostigmine in rats (Lesic & Varagic, 1961 ;Cass & Spriggs, 1961 ;Varagic & Vojvodid, 1962;Gokhale, Gulati & Joshi, 1963;Spriggs, 1966) and Spriggs (1966) additionally studied the inhibition of the contraction of the rat inferior eyelid caused by stimulation of the cervical sympathetic chain. Here is reported a study of the actions of bethanidine, bretylium, guanethidine, a-methyldopa, phenoxypropylguanidine (Chen, Ensor, McCarthy, McLean & Campbell, 1964) and reserpine on the pressor response to the ganglion stimulant, 4-(m-chlorophenylcarbomoyloxy)-2-butyryltrimethylammonium chloride (Roszkowski, 1961;Levy & Ahlquist, 1962;Murayama & Unna, 1963) in anaesthetized rats given a persistent ganglion blocking agent.…”

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confidence: 99%

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The Action of Adrenergic Neurone Blocking Agents and Other Drugs on the Pressor Responses of Various Agents in the Anaesthetized Rat

Robson

1967

British Journal of Pharmacology and Chemotherapy

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Section: Effects On Noradrenalinementioning

confidence: 95%

Section: Effects On Noradrenalinementioning

confidence: 99%

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confidence: 99%

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The Action of Adrenergic Neurone Blocking Agents and Other Drugs on the Pressor Responses of Various Agents in the Anaesthetized Rat

Robson

1967

British Journal of Pharmacology and Chemotherapy

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“…These workers, using a variety of sympathetically innervated preparations in acute and prolonged dosage experiments, showed that amphetamine and similar sympathomimetic amines antagonized the adrenergic neurone blockade produced by bretylium and guanethidine. Using the reduction in pressor responses of the rat to physostigmine as a measure of adrenergic neurone blockade, Gokhale, Gulati & Joshi (1965) and Spriggs (1966) showed that blockade was antagonized by sympathomimetic amines in this species. Spriggs (1966) also showed that the suppression by adrenergic neurone blocking agents of the contracture of the rat inferior eyelid to sympathetic nerve stimulation was antagonized by dexamphetamine.…”

Section: Introductionmentioning

confidence: 99%

The antagonism of adrenergic neurone blockade by amphetamine and dexamphetamine in the rat and guinea‐pig

Follenfant¹,

Robson²

1970

British J Pharmacology

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1. In isolated rat mesentery preparations, intra-arterial injection of the following drugs rapidly suppressed vasoconstrictor responses to sympathetic nerve stimulation: bretylium (75-100 ,g), guanethidine (10-20 p,g) and bethanidine (20-30 pg); with phenoxypropylguanidine (15-30 ,ug) the onset of blockade was slower. The blockade caused by these or higher concentrations was rapidly abolished by intra-arterial injection of amphetamine (100 Jug)as also was the blockade caused by infusing bretylium or guanethidine for 10-20 min. Partial blockade was produced by 20 ,ug of reserpine and this was only slightly and briefly antagonized by amphetamine. 2. In mesentery preparations taken from rats 24 h after subcutaneous injection of bretylium 50 mg/kg, guanethidine 10 mg/kg, phenoxypropylguanidine 10 mg/kg or reserpine 0-1 mg/kg, responses to sympathetic nerve stimulation were greatly impaired. Only in the preparations from the bretylium-treated rats did amphetamine antagonize the blockade. The adrenergic neurone blocking effect of bethanidine 10 mg/kg was evident at 12 h but not at 24 h after injection. 3. In rat mesentery amphetamine did not cause vasoconstriction but briefly potentiated the vasoconstrictor effect of sympathetic nerve stimulation. Responses to noradrenaline were not importantly affected. 4. The contractile responses of the rat inferior eyelid caused by stimulation of the cervical sympathetic nerve was greatly reduced 17-27 h after subcutaneous injection of bretylium 300 mg/kg, bethanidine 30 mg/kg, guanethidine 10 mg/kg or reserpine 0.3 mg/kg. Intravenous dexamphetamine (0-5 mg/kg) powerfully antagonized the effect of bretylium, weakly antagonized the blockade by bethanidine and guanethidine and caused no change in the response of reserpine-treated animals. 5. The vas deferens taken from guinea-pigs 24 h after subcutaneous injection of either bretylium or guanethidine showed greatly impaired responses to hypogastric nerve stimulation. Amphetamine largely restored the contractile response in bretylium-treated rats but caused only weak antagonism in the guanethidine-treated animals.

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“…Dexamphetamine is effective in reversing the adrenergic neurone blockade of guanethidine and similar drugs in many tissues (Day & Rand, 1963;Spriggs, 1966) including the vas of the mouse. In the present experiments dexamphetamine also reversed the inhibitory effect of atropine, but not that of lignocaine, phentolamine or pronethalol.…”

Section: Discussionmentioning

confidence: 99%

An Inhibitory Effect of Atropine on Responses of the Vas Deferens of the Mouse to Field Stimulation

Jones

Spriggs

1975

British J Pharmacology

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1 Atropine is shown to impair responses of the vas deferens of the mouse to field stimulation by acting at a site proximal to the smooth muscle cells. 2 The inhibitory effect of atropine is prevented by desmethylimipramine and reversed by dexamphetamine, and appears similar to the adrenergic-neurone blockade of guanethidine. 3 Electronmicroscopical studies show the presence in vas of presumptive noradrenergic axons which have acetylcholinesterase reaction product associated with their axolemmae. 4 These results are discussed in relation to the controversial hypothesis of a 'cholinergic link' in noradrenergic transmission.

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Peripheral Noradrenaline and Adrenergic Transmission in the Rat

Cited by 24 publications

References 24 publications

The Action of Adrenergic Neurone Blocking Agents and Other Drugs on the Pressor Responses of Various Agents in the Anaesthetized Rat

The Action of Adrenergic Neurone Blocking Agents and Other Drugs on the Pressor Responses of Various Agents in the Anaesthetized Rat

The antagonism of adrenergic neurone blockade by amphetamine and dexamphetamine in the rat and guinea‐pig

An Inhibitory Effect of Atropine on Responses of the Vas Deferens of the Mouse to Field Stimulation

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