ATROPINE‐RESISTANT EFFECTS OF THE MUSCARINIC AGONISTS McN‐A‐343 AND AHR 602 ON CARDIAC PERFORMANCE AND THE RELEASE OF NORADRENALINE FROM SYMPATHETIC NERVES OF THE PERFUSED RABBIT HEART

Fozard, John R.; Muscholl, E.

doi:10.1111/j.1476-5381.1974.tb08586.x

Cited by 15 publications

(15 citation statements)

References 17 publications

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“…One possible explanation for the effect of AHR-602 is the local anaesthetic action observed with high concentrations of the agonist (Fozard & Muscholl, 1974). The failure of AHR-602 to activate muscarinic receptors in the ear artery was in agreement with findings for prejunctional muscarinic receptors on sympathetic nerves in the rabbit heart (Fozard & Muscholl, 1972) but was unexpected given that McN-A-343 was an agonist in the ear artery.…”

Section: Discussionsupporting

confidence: 71%

“…AHR-602 produced some inhibition ofresponses to stimulation of the rabbit ear artery, but this was not exerted via activation of the prejunctional muscarinic receptor as the inhibition was unaffected by atropine in concentrations up to 100 nM. One possible explanation for the effect of AHR-602 is the local anaesthetic action observed with high concentrations of the agonist (Fozard & Muscholl, 1974). The failure of AHR-602 to activate muscarinic receptors in the ear artery was in agreement with findings for prejunctional muscarinic receptors on sympathetic nerves in the rabbit heart (Fozard & Muscholl, 1972) but was unexpected given that McN-A-343 was an agonist in the ear artery.…”

Section: Discussionmentioning

confidence: 99%

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Interaction of some muscarinic agonists and antagonists at the prejunctional muscarinic receptor in the rabbit ear artery preparation

Choo¹,

Mitchelson²,

Vong³

1986

British J Pharmacology

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1 The inhibitory effect of several muscarinic agonists on responses to sympathetic nerve stimulation of the isolated perfused ear artery of the rabbit was compared to that of acetylcholine in preparations pretreated with dyflos, cocaine and yohimbine. 2 In general the potency of the agonists was similar to that observed at peripheral muscarinic sites except for arecaidine propargyl ester and 4-(m-chlorophenylcarbamoyloxy)-2-butynyl trimethylammonium chloride

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Interaction of some muscarinic agonists and antagonists at the prejunctional muscarinic receptor in the rabbit ear artery preparation

Choo¹,

Mitchelson²,

Vong³

1986

British J Pharmacology

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“…Thus, it would be more appropriate to compare the stimulation-evoked 'H-overflow with the area under the time-tension curve. It has been suggested that McN-A-343 increased the release of NA from sympathetic nerves as a result of inhibition of transmitter re-uptake (Allen et al 1972;Fozard & Muscholl 1974;Nedergaard 1980a). Thus McN-A-343 inhibits the accumulation of 'H-NA by guinea-pig atria (Allen er af.…”

Section: Discussionmentioning

confidence: 99%

“…Thus McN-A-343 inhibits the accumulation of 'H-NA by guinea-pig atria (Allen er af. 1972), perfused rabbit heart (Fozard & Muscholl 1974) and rabbit aorta (Nedergaard 1980a). Evidence has been presented for the view that cocaine potentiates the contractile response of sympathetically innervated organs elicited by exogenous NA by inhibiting the uptake-I mechanism (Trendelenburg 1973).…”

Section: Discussionmentioning

confidence: 99%

“…butynyltrimethylammonium chloride] isa powerful stimulant of muscarine receptors in mammalian sympathetic ganglia (Roszkowski 1961), while it has little action at classical peripheral muscarine receptors (Roszkowski 1961;Fozard & Muscholl 1974;Hobbiger et al 1969;Pappano & Rembish 1971;Smith 1966). Muscarinic agonists reduce the stimulation-evoked release of transmitter from many sympathetically innervated tissues (for reviews, see Starke 1977;Westfall 1977;Langer 1977;Muscholl 1979;Vizi 1979).…”

Section: Mcn-a-343 [4-(rn-chlorphenylcarbamoyloxy)-6-mentioning

confidence: 99%

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Dual Effect of the Muscarinic Agonist McN‐A‐343 on Vascular Neuroeffector Transmission

Nedergaard

1981

Acta Pharmacologica et Toxicologica

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The site and mechanism of action of McN‐A‐343 (4‐m‐chlorophenylcarbamoyloxy)‐2‐butynyltrime‐thylammonium chloride) on sympathetic neuroeffector transmission in the rabbit isolated pulmonary artery was studied. Low concentrations (10−6 — 3 × 10−5 M) of McN‐A‐343 and cocaine enhanced (up to 210 and 236%, respectively) the contractions evoked by electrical‐field stimulation, while higher concentrations (10−4 — 3 × 10−4 M) inhibited them. McN‐A‐343 (10−4 M) caused an initial transitory potentiation (222% of control) of the stimulation‐evoked contractions followed by an inhibition. In the presence of cocaine (3 × 10−5 M), the potentiation caused by McN‐A‐343 was prolonged and the secondary inhibitory phase was thus abolished. Physostigmine (10−5 — 10−4 M), hexamethonium (10−5 M), atropine (3 × 10−7 M), suprofen (10−5 M), and 4‐aminopyridine did not alter the effect of McN‐A‐343 (10−4 M). Cocaine (3 × 10−5 M)and(+)‐amphetamine (10−5 M) reversed the McN‐A‐343‐evoked block, while they did not alter the inhibition caused by tetracaine (3.2 × 10−5 M). Atropine (3 × 10−7 M) had no effect on the McN‐A‐343‐induced block, while 4‐aminopyridine (10−4 M) caused a partial and transitory reversal. On the aorta McN‐A‐343 (10−4 M) did not alter the contractile concentration‐response curve of (—)‐noradrenaline (10−9 — 3 × 10−4 M), while that of serotonin (10−8 — 3 × 10−5 M) was moved to the right in a competitive manner. McN‐A‐343 (10−4 M) did not alter the contractions evoked by noradrenaline (10−7 M) during the period corresponding to the stimulation‐evoked enhancement and subsequent inhibition. McN‐A‐343 (10−4 M) slightly antagonized the contractions caused by tyramine (10−6 — 10−3 M) and carbachol (10−6 — 10−3 M). It is concluded that McN‐A‐343 enhances stimulation‐evoked transmitter release by a presynaptic facilitatory action mediated via receptors localized on the outer surface of adrenergic neurones and to a lesser extent by inhibition of noradrenaline re‐uptake. The enhancement does not involve presynaptic nicotine or muscarine receptors. Furthermore, McN‐A‐343 inhibits transmitter release by acting as an adrenergic neurone blocking agent at an intraneuronal site. The inhibition does not involve presynaptic muscarine inhibitory receptors and is prostaglandin‐independent.

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Sphincteric function

Papasova

1989

Comprehensive Physiology

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ATROPINE‐RESISTANT EFFECTS OF THE MUSCARINIC AGONISTS McN‐A‐343 AND AHR 602 ON CARDIAC PERFORMANCE AND THE RELEASE OF NORADRENALINE FROM SYMPATHETIC NERVES OF THE PERFUSED RABBIT HEART

Cited by 15 publications

References 17 publications

Interaction of some muscarinic agonists and antagonists at the prejunctional muscarinic receptor in the rabbit ear artery preparation

Interaction of some muscarinic agonists and antagonists at the prejunctional muscarinic receptor in the rabbit ear artery preparation

Dual Effect of the Muscarinic Agonist McN‐A‐343 on Vascular Neuroeffector Transmission

Sphincteric function

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