Regional differences in the response to nicotine in isolated canine arteries

Toda, Noboru

doi:10.1016/0014-2999(76)90310-1

Cited by 20 publications

(7 citation statements)

References 10 publications

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“…It has been reported that the responses of isolated strips of cerebral blood vessels to nicotine vary according to species of animals: relaxation in dogs [18,19], contraction in humans [15] and no response in cattle [15]. The present experiments show that nicotine has dual actions on dog cerebral arteries and that there is a difference in the response of the basilar and middle cerebral arteries.…”

Section: Discussionsupporting

confidence: 50%

Vasoconstrictor and Dilator Actions of Nicotine and Electrical Transmural Stimulation on Isolated Dog Cerebral Arteries

Muramatsu¹,

Fujiwara²,

Osumi³

et al. 1978

J Vasc Res

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Effects of nicotine and electrical transmural stimulation on isolated dog cerebral arteries were studied. Nicotine (5 × 10^–8–10^–4 m) usually evoked a phasic contraction in the basilar artery and a relaxation in the middle cerebral artery. The nicotine-induced contraction and relaxation were abolished by pretreatment with pentolinium (10^–5 m) but not by tetrodotoxin (TTX) (10^–7 m). Phentolamine (10^–6 m) or bretylium (10^–5 m) abolished or reversed the nicotine-induced contraction, and partially reduced the nicotine-induced relaxation. Electrical transmural stimulation elicited a phasic contraction in the basilar artery and a relaxation or slight contraction in the middle cerebral artery. The contraction induced by transmural stimulation was abolished by bretylium and TTX, and augmented by phentolmine. The relaxation was not inhibited by bretylium. The uptake of ³H-norepinephrine (³H-NE) by the basilar and middle cerebral arteries was markedly reduced by cocaine (3 × 10^–6 m). Nicotine and transmural stimulation increased the tritium efflux from both arteries. The nicotine-induced increase in tritium efflux was inhibited by pentolinium. The increased efflux induced by transmural stimulation was abolished by TTX, attenuated by bretylium, and augmented by phentolamine. These results indicate that nicotine and transmural stimulation cause both vasoconstrictor and vasodilator effects in the dog cerebral arteries and that the vasoconstriction is mediated through an adrenergic mechanism.

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Section: Discussionsupporting

confidence: 50%

Vasoconstrictor and Dilator Actions of Nicotine and Electrical Transmural Stimulation on Isolated Dog Cerebral Arteries

Muramatsu¹,

Fujiwara²,

Osumi³

et al. 1978

J Vasc Res

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“…Previous attempts to stimulate such nerves in isolated coronary arteries have generally been unsuccessful (Nishioka, 1971;Toda, 1975); however, more recently it has been reported that adrenergic responses can be elicited in the isolated left descending coronary artery of the dog when stimulating electrodes are placed close to the aortic root (Borda, Schuchleib & Henry, 1977). (Furchgott, 1972).…”

Section: Discussionmentioning

confidence: 99%

Effects of Uptake Inhibitors on Responses of Sheep Coronary Arteries to Catecholamines and Sympathetic Nerve Stimulation

Brine¹,

Cornish²,

Miller³

1979

British J Pharmacology

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1 Transmural stimulation of intrinsic sympathetic nerves and exogenous catecholamines produce /I-adrenoceptor mediated relaxant responses in strips of contracted sheep coronary artery.2 The neuronal uptake inhibitors, metaraminol, cocaine and desipramine and the extraneuronal uptake inhibitor, cortisol, failed to potentiate responses to noradrenaline or sympathetic stimulation; responses to isoprenaline were enhanced by cortisol. 3 Oxytetracycline, which inhibits binding to connective tissue fibres, did not affect responses to noradrenaline or nerve stimulation. 4 17,B-Oestradiol, caffeine and U0521 proved to be unsuitable compounds for studying catecholamine inactivation since they non-selectively potentiated responses to noradrenaline and isoprenaline. 5 It is concluded that catecholamine inactivation processes do not modify transmitter function in sheep coronary arteries.

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“…From studies on isolated cerebral arteries of the dog in response to nicotine (Toda, 1975;1976a) and on cat, dog and sheep cerebral arteries in response to transmural electrical stimulation (Lee, Su & Bevan, 1975; Duckles, 1979), a non-adrenergic, non-cholinergic mechanism of relaxation induced by nerve stimulation has been postulated. Such a relaxation was not observed in cerebral arteries isolated from monkeys (Duckles, Lee & Bevan, 1977).…”

Section: Introductionmentioning

confidence: 99%

Non‐adrenergic, Non‐cholinergic Innervation in Monkey and Human Cerebral Arteries

Toda

1981

British J Pharmacology

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1Transmural electrical stimulation (0.5 to 20 Hz) and nicotine (10' M) produced relaxations of helically-cut strips of monkey and human cerebral arteries, contracted with prostaglandin F22. 2 The relaxation induced by electrical stimulation was suppressed or abolished by tetrodotoxin, while the nicotine-induced relaxation was abolished by hexamethonium but was unaffected by tetrodotoxin. Both relaxations were not attenuated by ,B-adrenoceptor antagonists and atropine. 3 These findings may indicate that large cerebral arteries of the monkey and man are innervated by non-adrenergic, non-cholinergic nerves, excitation of which liberates unknown vasodilator substance(s).

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Regional differences in the response to nicotine in isolated canine arteries

Cited by 20 publications

References 10 publications

Vasoconstrictor and Dilator Actions of Nicotine and Electrical Transmural Stimulation on Isolated Dog Cerebral Arteries

Vasoconstrictor and Dilator Actions of Nicotine and Electrical Transmural Stimulation on Isolated Dog Cerebral Arteries

Effects of Uptake Inhibitors on Responses of Sheep Coronary Arteries to Catecholamines and Sympathetic Nerve Stimulation

Non‐adrenergic, Non‐cholinergic Innervation in Monkey and Human Cerebral Arteries

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