Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

Wetzel, Glenn T.; Brown, JT

doi:10.1152/ajpheart.1985.248.1.h33

Cited by 46 publications

(40 citation statements)

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“…Such receptors have previously been described in the cardiac nerves in the rat (Wetzel & Brown, 1985) and in the guinea-pig (Jeck et al, 1988). Blockade of these receptors by gallamine would increase transmitter output from the vagus nerves and increase the concentration of antagonist required to inhibit vagallyinduced bradycardia.…”

Section: Discussionmentioning

confidence: 86%

Effect of pirenzepine and gallamine on cardiac and pulmonary muscarinic receptors in the rabbit

Maclagan

Faulkner

1989

British J Pharmacology

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1 The effect of muscarinic antagonists considered to be selective for M1 receptors (pirenzepine) and for M2 receptors (gallamine) were studied on bronchoconstriction and bradycardia elicited by stimulation of the vagal nerves and by i.v. acetylcholine (ACh) in anaesthetized rabbits. 2 Pirenzepine was equipotent as an antagonist of ACh-induced responses at postjunctional muscarinic receptors in the heart, lung and blood vessels, whereas gallamine was at least ten times less potent at pulmonary and vascular muscarinic receptors. Thus, gallamine never caused complete inhibition of bronchoconstrictor or hypotensive responses to i.v. ACh, whereas doses of pirenzepine in excess of 1 pmol kg1-abolished all muscarinic responses. 3 In the lung, both antagonists inhibited bronchoconstriction caused by vagal stimulation and ACh-induced bronchoconstriction to the same extent (pirenzepine, mean ED50 65 + 22 and 130 + 28nmolkg-1 respectively; gallamine, ED50> 10,OOOnmolkg-1 for both responses).Enhancement of vagally-induced bronchoconstriction was never observed. 4 In the heart, however, both pirenzepine and gallamine were ten times less potent as antagonists of vagally-induced bradycardia than of ACh-induced bradycardia. This differential blockade was unaltered by propranolol (1 mg kg-1) pretreatment. 5 It is concluded that there is no evidence for M1 or M2 muscarinic receptors in the pulmonary innervation of the rabbit and the potency of the antagonists in abolishing vagally-induced bronchoconstriction was consistent with blockade of M3 muscarinic receptors on airway smooth muscle. 6 The results suggest that M2 muscarinic receptors may exert an inhibitory effect on transmission in the parasympathetic nerves innervating the heart in the rabbit. Blockade of such neuronal receptors would increase transmitter output to the atrial cells and explain the low potency of both antagonists in abolishing vagally-induced bradycardia in the rabbit.

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Section: Discussionmentioning

confidence: 86%

Effect of pirenzepine and gallamine on cardiac and pulmonary muscarinic receptors in the rabbit

Maclagan

Faulkner

1989

British J Pharmacology

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“…This result is in keeping with previous studies which have shown that low-dose atropine amplifies vagal cardiac efferent activity (16, 17). Previous studies have demonstrated that the negative chronotropic action of atropine is mediated by both central (18, 19) and peripheral (20)(21)(22) mechanisms. Vertebral interspace variation in the antimuscarinic action of atropine, the effects of anesthesia, and the doses of atropine used in the studies make it difficult to extrapolate previously obtained results to human studies.…”

Section: Effects Of Low-dose Atropine On Cardiac Vagal Activitymentioning

confidence: 99%

Low-Dose Atropine Attenuates Muscle Sympathetic Nerve Activity in Healthy Humans.

et al. 2000

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and Ken-ichi KOBAYASHI Central muscarinic receptors play an important role in the regulation of cardiac vagal nerve activity. We studied the inhibition of central muscarinic receptors and sympathetic nerve function in humans, since very little information is currently available on this subject. We examined the effects of graded doses of atropine (five doses, range 0.001 to 0.016 mg/kg) on heart rate, arterial pressure, heart rate variability, and muscle sympathetic nerve activity in 13 healthy young volunteers. Atropine caused biphasic effects on heart rate and the high-frequency (HF) power of R-R interval variability. At lower doses (0.002 mg/kg for heart rate, 0.001 mg/kg for HF power), atropine decreased heart rate and increased HF power. In contrast, at higher doses, atropine increased heart rate and decreased HF power. Low-dose atropine significantly attenuated muscle sympathetic nerve activity, burst rate (bursts/min) by -30.5±6.0% and burst incidence (bursts/100 heart beats) by -23.8 ± 6.9% at 0.002 mg/kg. Systolic and diastolic arterial pressure did not change with atropine infusion. Low-dose atropine (0.002 mg/kg) did not significantly affect either low frequency (LF) power or LF/HF. These results suggest that central muscarinic receptors may modulate not only cardiac vagal nerve activity but also sympathetic nerve activity in the skeletal muscle vasculature.

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“…In these tissues, the receptors are located in the ganglia (Suzuki & Volle, 1979;Gallagher et al, 1982;Morita et al, 1982;Ashe & Yarosh, 1984) and on the postganglionic final nerve terminals (Loffelholz & Muscholl, 1970;Kilbinger & Wagner, 1979;Fox et al, 1985;Wetzel & Brown, 'Author for correspondence. 1985).…”

Section: Introductionmentioning

confidence: 99%

Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

Faulkner

Fryer

Maclagan

1986

British J Pharmacology

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1 The location of neuronal inhibitory muscarinic receptors in pulmonary parasympathetic nerves was investigated in vivo and in vitro. The effects of an agonist for neuronal muscarinic receptors (pilocarpine) and an antagonist (gallamine) were tested on contractions of airway smooth muscle induced by pre-and postganglionic cholinergic nerve stimulation. 2 In anaesthetized guinea-pigs, gallamine potentiated constriction of the tracheal tube and smaller airways induced by preganglionic stimulation. Gallamine also potentiated postganglionic stimulation induced by transmural stimulation of the tracheal tube and by 1-1-dimethyl-4-phenylpiperazinium iodide in the rest of the lung. 3 Bronchoconstriction and contraction of the tracheal tube induced by intravenous acetylcholine were not potentiated by gallamine, indicating that postjunctional muscarinic receptors in airway smooth muscle were not involved in the potentiation. 4 The muscarinic agonist, pilocarpine, had the opposite effect to gallamine and inhibited contractions of the tracheal tube induced by both types of nerve stimulation. 5 In vitro, the inhibitory effect of pilocarpine was demonstrated in the tracheal tube preparation stimulated both pre-and postganglionically. The effect of pilocarpine was antagonized by gallamine. 6 Because gallamine and pilocarpine affected the responses to postganglionic stimulation, the inhibitory muscarinic receptors must be located on the postganglionic neurones of the parasympathetic nerves innervating the trachea and the smaller airways. However, these experiments cannot exclude the possibility that muscarinic receptors may also be located on the soma of the ganglion cells.

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Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

Cited by 46 publications

References 0 publications

Effect of pirenzepine and gallamine on cardiac and pulmonary muscarinic receptors in the rabbit

Effect of pirenzepine and gallamine on cardiac and pulmonary muscarinic receptors in the rabbit

Low-Dose Atropine Attenuates Muscle Sympathetic Nerve Activity in Healthy Humans.

Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

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