Sensory Mechanisms Involved in the Bezold‐jarisch Effect

Paintal, A. S.

doi:10.1038/icb.1973.1

Cited by 13 publications

(5 citation statements)

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“…Indeed, with the exception of Gupta & Thames (1983), investigators have identified comparatively few ventricular receptors with myelinated fibres (Paintal, 1955;Coleridge et al 1964;Oberg & Thoren, 1972;Baker et al 1979;Thoren, 1979), even though single-unit activity is recorded more easily from myelinated than from non-myelinated fibres. Despite the apparent scarcity of ventricular receptors with myelinated fibres, Paintal (1955Paintal ( , 1973 has suggested that these afferent endings are largely responsible for triggering the Bezold-Jarisch reflex. Paintal's suggestion is consistent with the observation that the reflex is abolished by cooling the vagus nerves to 8°C (Dawes et al 1951;Sleight, 1964), a temperature at which it is generally agreed that impulse conduction in myelinated vagal axons is largely blocked, whereas that in nonmyelinated axons is only partially attenuated (Franz & Iggo, 1968;Jonzon et al 1988).…”

Section: Afferent Pathwaysmentioning

confidence: 99%

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

Clozel¹,

Pisarri²,

Coleridge³

et al. 1990

The Journal of Physiology

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SUMMARY1. Veratridine injected into the coronary circulation stimulates afferent vagal endings in the heart to evoke bradycardia and systemic hypotension (Bezold-Jarisch reflex, coronary chemoreflex) and coronary vasodilatation. We have examined certain features of the reflex coronary vasodilator response in anaesthetized dogs.2. When the circumflex coronary artery was perfused at constant pressure (100 mmHg), injection of veratridine (03 Ig kg-1) into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex blood flow by 54 %; when heart rate was kept constant, circumflex flow increased by 57 %. The increase in circumflex flow was reduced 63 % by atropine, and finally abolished by phentolamine. 3. During severe coronary underperfusion (perfusion pressure 45 mmHg), veratridine still increased coronary flow by 35 %, an increase amounting to 24-64 % of the coronary vascular reserve. Flow increased in all layers of the myocardium, but the relative distribution of flow between subendocardial and subepicardial layers was unaltered.4. Veratridine stimulates both mechanosensitive and chemosensitive cardiac endings. Stimulating chemosensitive afferents selectively by injecting capsaicin (1V5 jug kg-') into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex flow by 50 % (and by 36 % when heart rate was kept constant).5. In ten of fifteen dogs, veratridine and capsaicin still evoked coronary vasodilatation when vagal A fibres were blocked selectively by cooling to 7 5°C, the increase in coronary flow averaging 45 % of that at 37 'C. All responses were abolished by cooling to 0 'C.6. We conclude that coronary vasodilatation can be evoked by selective stimulation of cardiac chemosensitive vagal C fibres, although the coronary vasodilatation of the veratridine-induced Bezold-Jarisch reflex may be due to stimulation of both mechanosensitive and chemosensitive C fibres. We speculate that during periods of coronary underperfusion ischaemic stimulation of chemosensitive vagal C fibres evokes a reflex dilatation of the coronary vascular bed that supplements the dilatation dependent upon autoregulatory mechanisms. MUS 8253 J. P. CLOZEL AND OTHERS

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Section: Afferent Pathwaysmentioning

confidence: 99%

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

Clozel¹,

Pisarri²,

Coleridge³

et al. 1990

The Journal of Physiology

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“…Vagal afferent traffic from cardiac receptors stimulated by veratrum alkaloids has been extensively studied by numerous investigators and has been reviewed by Paintal (24,25). Intracoronary administration of veratridine stimulates a variety of receptors with different afferent fiber size.…”

Section: Figurementioning

confidence: 99%

Reflex parasympathetic coronary vasodilation elicited from cardiac receptors in the dog.

Feigl¹

1975

Circulation Research

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Veratrum alkaloids injected into the coronary circulation stimulate myocardial receptors to produce reflex bradycardia and arterial hypotension (the Bezold-Jarisch reflex). This study investigated the hypothesis that parasympathetic coronary vasodilation occurs as part of the Bezold-Jarisch reflex. Blood flow in the circumflex coronary artery was measured in chloralose-anesthetized, closed-chest dogs with a newly developed cannula-tip flow transducer. Alpha-receptor blockade with Dibozane (2 mg/kg) was used to prevent peripheral vasodilation, and beta-receptor blockade with propranolol (1 mg/kg) was used to prevent adrenergic cardiac effects. Electrical pacing was used to maintain a constant heart rate. Under these conditions, veratridine injected into the anterior descending coronary artery but not into the circumflex coronary artery produced a 63% increase in circumflex coronary blood flow and an 88% increase in diastolic coronary conductance. The effect was abolished when the reflex arc was interrupted by either vagotomy or atropine administration. It is concluded that a cardiocoronary reflex parasympathetic coronary vasodilation can be elicited by stimulating cardiac receptors with veratridine.• In 1867 Bezold and Hirt (1) described bradycardia and arterial hypotension following intravenous injections of veratrum alkaloids. Jarisch and co-workers (2-4) established that the sensory receptors for this response are in the heart and the afferent path is the vagus nerve. Krayer (5) reviewed the history of the reflex and proposed that it be called the Bezold-Jarisch effect.A previous study in this laboratory demonstrated that stimulation of the efferent vagus nerve results in parasympathetic coronary vasodilation which is independent of the inotropic and chronotropic effects of vagal stimulation (6). The present study was designed to test whether reflex parasympathetic coronary vasodilation is part of the BezoldJarisch reflex. The plan of the experiment was to observe circumflex coronary artery blood flow during injection of veratridine into the anterior descending and septal coronary arteries before and after interruption of the postulated reflex arc. Methods GENERAL PREPARATIONAdult male dogs (23-27 kg) were medicated with morphine sulfate (2.5 mg/kg, sc) and anesthetized with alpha-chloralose (50 mg/kg, iv), with supplements given as needed. The dogs were mechanically ventilated via a

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“…In addition to 5-HT, 2-methyl-5-HT, a selective 5-HT3-receptor agonist, has also been reported to evoke BJR (13). Paintal (14) reported that 5-HT-sensitive receptors (chemoreceptor-like tissues) and veratridine-sensitive chemoreceptors are located in the same area in the heart, indicating that 5-HT might act not only 5-HT3 receptors but also on chemoreceptors on the endings of afferent vagus nerves. In the present study, therefore, we evaluated the inhibitory effects of YM060 and YM114 on BJR induced by 2-methyl-5-HT in anesthetized rats and compared the results with those of ondansetron and granisetron.…”

Section: Bjr Induced By 5-ht Injected Into the Left Ventriclementioning

confidence: 99%

“…These responses are mediated by ACh released from the endings of vagal efferent nerves. In anesthetized cats, dogs and rats, intraventricular and intravenous injection of veratridine stimulates the vagus nerves through activation of chemoreceptors and baroreceptors located in the heart, resulting in bradycardia and hypotension (14)(15)(16)(17). In the present study, intravenous veratridine, like 5-HT and 2-methyl-5-HT, dose-dependently produced transient bradycardia in anesthetized rats.…”

Section: Bjr Induced By 5-ht Injected Into the Left Ventriclementioning

confidence: 99%

“…Bradycardiac reflex through the stimulation of vagus nerves is evoked not only by activation of 5-HT3 receptors but also by activation of chemoreceptors in the heart and electrical stimulation of vagus nerves. It was reported that veratridine-induced BJR was evoked by ACh released from vagal efferent nerves through activation of chemoreceptors and baroreceptors located on the endings of vagal afferent nerves in the heart (14)(15)(16)(17). Therefore, bradycardia induced by 5-HT, veratridine or electrical stimulation of vagus nerves is inhibited by anti-cholinergic agents, nicotine-receptor antagonists, local anesthetics and Na+-channel blockers.…”

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confidence: 99%

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Characteristics of Inhibitory Effects of Serotonin (5-HT)3-Receptor Antagonists, YM060 and YM114 (KAE-393), on the von Bezold-Jarisch Reflex Induced by 2-Methyl-5-HT, Veratridine and Electrical Stimulation of Vagus Nerves in Anesthetized Rats

Yamano¹,

Ito²,

Kamato³

et al. 1995

Japanese Journal of Pharmacology

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BJR were largely consistent with those against 5-HT-induced BJR. In contrast, higher doses (100 pg/kg, i.v.) of YM060, YM114, ondansetron and granisetron did not inhibit veratridine (150 pg/kg, i.v.)-induced BJR. Atropine (300 pg/kg, i.v.) abolished bradycardia induced by electrical stimulation of vagal efferent nerves, whereas YM060, YM 114, ondansetron and granisetron had no effect at a dose of 1000 ug/kg, i.v. 5-HT (0.625-5.0 pg) injected into the left ventricle also caused a dose-dependent decrease in heart rate, an effect that was abolished by YM060 (0.1 pg/kg, i.v.), atropine (100 pg/kg, i.v.) and vagotomy. These results suggest that YM060 and YM114 are highly potent and selective 5-HT3-receptor antagonists that do not affect veratridine-or electrical stimulation-induced bradycardia in anesthetized rats. They also suggest that 5-HT-induced BJR in anesthetized rats originates from 5-HT3 receptors located on the endings of vagal afferent nerves in the heart. Keywords: 5-HT3-receptor antagonist, von Bezold-Jarisch reflex, Vagus nerve, Veratridine Serotonin (5-HT) is widely distributed and is implicated in a variety of physiological responses. Research into 5-HT-receptor subtypes, especially the 5-HT3 receptor, has advanced in recent years. 5-HT3 receptors are located on central, sensory and autonomic nerves and on the myenteric plexus (1, 2), and have been implicated in anxiety (3, 4), vomiting responses to cancer chemotherapeutic agents (5, 6) and stress-induced gastrointestinal disorders (7).Bolus intravenous injection of 5-HT causes transient bradycardia (the von Bezold-Jarisch reflex; BJR) in many species including rats, cats, dogs and rabbits (8-11). Fozard (12) reported that this reflex in anesthetized rats is mediated through the activation of 5-HT3 receptors located on endings of vagal afferent nerves. Activation of these receptors lead to the stimulation of vagus nerves, resulting in the bradycardia. 5-HT1-and 5-HT2-receptor antagonists had no effects on BJR induced by 5-HT in anesthetized rats (13). BJR in anesthetized rats is therefore frequently utilized as an in vivo system for the evaluation of 5-HT3-receptor blocking effects. Bradycardiac reflex through the stimulation of vagus nerves is evoked not only by activation of 5-HT3 receptors but also by activation of chemoreceptors in the heart and electrical stimulation of vagus nerves. It was reported that veratridine-induced BJR was evoked by ACh released from

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Sensory Mechanisms Involved in the Bezold‐jarisch Effect

Cited by 13 publications

References 3 publications

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

Reflex parasympathetic coronary vasodilation elicited from cardiac receptors in the dog.

Characteristics of Inhibitory Effects of Serotonin (5-HT)3-Receptor Antagonists, YM060 and YM114 (KAE-393), on the von Bezold-Jarisch Reflex Induced by 2-Methyl-5-HT, Veratridine and Electrical Stimulation of Vagus Nerves in Anesthetized Rats

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