MDL 72222 (a selective 5‐HT3 receptor antagonist) prevents stimulation of intrapulmonary C fibres by pulmonary embolization in anaesthetized rabbits

Kay, IS; Armstrong, DJ

doi:10.1113/expphysiol.1991.sp003487

Cited by 12 publications

(5 citation statements)

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“…Earlier evidence revealed that MDL precluded serotonin-induced chemoexcitation of carotid body chemoreceptors in cats and reflex apnea provoked by 5HT 3 agonist in rats (Kirby and McQueen, 1984;McQueen et al, 1998). Qualitatively similar results were obtained in rabbits since a large dose of MDL attenuated tachypnoea in experimental pulmonary embolism, reduced respiratory effects of the intravenous 5HT and blocked stimulation of vagal C-fibers endowed with 5HT 3 receptors Kay and Armstrong, 1990;Kay and Armstrong, 1991). It is of note that in our study, respiratory reflex responses triggered by excitation of 5HT 3 receptors were potently, completely inhibited by MDL.…”

Section: Discussionsupporting

confidence: 71%

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5HT2 and 5HT3 receptors' contribution to modeling of post-serotonin respiratory pattern in cats

Kopczyńska

Szereda-Przestaszewska

2004

Life Sciences

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Section: Discussionsupporting

confidence: 71%

“…It has been shown that the respiratory effects of 5HT are due to stimulation of pulmonary C fibers endings, endowed with 5HT 3 receptors in rabbits Kay and Armstrong, 1991). Moreover, 5HT 2 and 5HT 3 receptors are present on sensory cell bodies in the nodose ganglion in this species (Christian et al, 1989).…”

Section: Introductionmentioning

confidence: 98%

5HT2 and 5HT3 receptors' contribution to modeling of post-serotonin respiratory pattern in cats

Kopczyńska

Szereda-Przestaszewska

2004

Life Sciences

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“…Experimental pulmonary embolism in rabbits leads to serotonin release (presumably from platelets) that in turn stimulates 5‐HT3 receptors on intrapulmonary vagal C‐fibres causing reflex tachypnoea (Armstrong & Kay, 1990). Intrapulmonary entrapment of activated platelets leads to reflex‐mediated circulatory collapse in part due to 5‐HT3 receptor‐mediated afferent nerve activation (Kay & Armstrong, 1991). Based on present findings, it would appear that these processes probably involve the activation of nodose more than jugular intrapulmonary vagal C‐fibres.…”

Section: Discussionmentioning

confidence: 99%

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Potenzieri¹,

Meeker²,

Undem³

2012

The Journal of Physiology

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Key points• Mast cell-derived serotonin is a principal mediator of allergic reactions in rodents. Serotonin can also be released from platelets during various pathological conditions. • Vagal C-fibres innervating the respiratory tract can be subdivided into nodose (placodal) C-fibres or jugular (neural crest) C-fibres). Activation of vagal placodal and/or neural crest vagal C-fibres probably contributes to the dyspnoea, cough and reflex parasympathetic drive commonly associated with serotonin.• Serotonin used different receptor subtypes to evoke strong action potential discharge in placodal (5-HT3 receptors) versus neural crest (non-5-HT3 receptors)-derived vagal C-fibres in the mouse lung.• Mast cell derived serotonin may activate neural crest C-fibres, but did not stimulate placodal C-fibres.• The effect of extracellular serotonin on vagal afferent activation therefore depends on its cellular source and the C-fibre phenotype.Abstract The effect of serotonin on capsaicin-sensitive vagal C-fibre afferent nerves was evaluated in an ex vivo vagally innervated mouse lung preparation. Action potentials arising from receptive fields in the lungs were recorded with an extracellular electrode positioned in the nodose/jugular ganglion. Among the 62 capsaicin-sensitive C-fibres studied (conduction velocity ∼0.5 m s −1 ), 71% were of the nodose phenotype and 29% of the jugular phenotype. The nodose C-fibres responded strongly to serotonin and this effect was blocked with the 5-HT3-receptor antagonist ondansetron. Using single cell RT-PCR, we noted that the vast majority of nodose neurons retrogradely labelled from the lung, expressed 5-HT3 receptor mRNA. The jugular C-fibres also responded strongly to serotonin with action potential discharge, but this effect was not inhibited by ondansetron. Lung-specific jugular neurons did not express 5-HT3 receptor mRNA but frequently expressed 5-HT1 or 5-HT4 receptor mRNA. Mast cells are the major source of serotonin in healthy murine airways. Ovalbumin-induced mast cell activation in actively sensitized lungs caused action potential discharge in jugular but not nodose C-fibres. The data show that vagal C-fibres in the respiratory tract of the mouse are strongly activated by serotonin. Depending on the C-fibre subtype both 5-HT3 and non-5-HT3 mechanisms are involved.

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“…As mentioned in the introduction, serotonin likely stimulates C fibre sensory afferents. Administered into the pulmonary circulation, it excites vagal C fibres endowed with 5HT 3 receptors [14,17,23] and increases the activity of the serotonergic system throughout the whole vagal pathway to the nucleus of the solitary tract [10]. In the present experiments, disruption of this afferent input from the lungs at the midcervical level reduced both the size and duration of the ventilatory responses to serotonin, but did not qualitatively alter the pattern of the respiratory sequelae.…”

Section: Discussionmentioning

confidence: 62%

“…This constellation of cardiorespiratory responses has been termed pulmonary chemoreflex [6]. It has been shown that the respiratory effects of 5HT are due to stimulation of pulmonary C fibre endings, endowed with 5HT 3 receptors [3,17] in cats and rabbits; however, 5HT is acting at reduced level following midcervical section of the vagi [8]. Moreover, apnoea induced by injecting 5HT into the common carotid artery is abolished by supranodose vagotomy in cats [4,16].…”

Section: Introductionmentioning

confidence: 99%

Supranodose Vagotomy Precludes Reflex Respiratory Responses to Serotonin in Cats

Kopczyńska¹,

Szereda-Przestaszewska²

2003

J Biomed Sci

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Mediation of the respiratory reflex effects of an exogenous serotonin challenge goes beyond the lung vagi and is suggested to involve the nodose ganglia. In the present experiments the effects of an intravenous serotonin challenge on breathing pattern were studied in 8 pentobarbitone-chloralose anaesthetised cats. Bolus injection of serotonin oxalate (50 µg/kg) into the right femoral vein evoked prompt apnoea of 19.2 (± 2.4)-second duration in all 8 cats while intact; the apnoea was much shorter after midcervical vagal section (8.1 ± 0.9 s, p < 0.001), and was abolished by supranodose vagotomy. In post-apnoeic breaths, the tidal volume was reduced from a baseline of 34.1 ± 4.0 to 13.5 ± 1.1 ml (p < 0.001) prior to, and from a baseline of 43.9 ± 5.4 to 33.8 ± 6.6 ml (p < 0.01) after midcervical vagotomy; the serotonin challenge did not affect tidal volume following supranodose vagal section (p = 0.4). The increase in respiratory rate found in intact (p < 0.001) and midcervically vagotomised cats (p < 0.01) was eliminated by the neurotomy above the nodose ganglia. Supranodose vagotomy altered cardiovascular response to serotonin by replacing the fall in blood pressure with an increase. These data suggest that the sequelae of serotonin-induced pulmonary chemoreflex, i.e. respiratory arrest, cardiovascular changes and post-apnoeic pattern of breathing require intact nodose ganglia.

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MDL 72222 (a selective 5‐HT3 receptor antagonist) prevents stimulation of intrapulmonary C fibres by pulmonary embolization in anaesthetized rabbits

Cited by 12 publications

References 12 publications

5HT2 and 5HT3 receptors' contribution to modeling of post-serotonin respiratory pattern in cats

5HT2 and 5HT3 receptors' contribution to modeling of post-serotonin respiratory pattern in cats

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Supranodose Vagotomy Precludes Reflex Respiratory Responses to Serotonin in Cats

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