Bradykinin stimulates respiratory drive by activating pulmonary  sympathetic afferents in the rabbit

Soukhova, G.; Wang, Y.; Ahmed, Muhammad; Walker, Jeffery W.; Yu, Jerry

doi:10.1152/japplphysiol.00582.2002

Cited by 20 publications

(13 citation statements)

References 32 publications

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“…Reflex effects on breathing pattern appear in another report (26). The reflex effects are primarily initiated through sympathetic afferent rather than vagal afferent pathways, because they persisted after bilateral vagotomy (present results) and can be blocked by bilateral section of sympathetic chains and white rami (26). The depressor effects on hemodynamics may result from withdrawing sympathetic efferent activity.…”

Section: Discussionsupporting

confidence: 53%

“…2). Reflex effects on respiratory drive occurred in most but not all cases (26). Reflex hemodynamic effects showed a depressor response in 38 of 59 trials on 18 rabbits (64%).…”

Section: Resultsmentioning

confidence: 93%

“…Phrenic efferent nerve activity was recorded from C6 (right or left) to assess central inspiratory drive. In some experiments, the electrical activity of the abdominal muscles (external oblique) was recorded to assess expiratory drive (26). These measured variables, together with airway pressure and RSNA, were recorded by a thermorecorder (Dash IV, Astro-Med).…”

Section: Methodsmentioning

confidence: 99%

“…This afferent activity increases during lung inflation (12). Activation of pulmonary sympathetic afferents may excite (26) or inhibit breathing (11). Stimulation of cardiopulmonary sympathetic afferents can produce a depressor response in monkeys and dogs (10), and produces either depressor or pressor responses in cats (31).…”

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confidence: 99%

“…In the present study, the reflex effects of activating pulmonary sympathetic afferents on hemodynamics were evaluated by directly injecting bradykinin into the lung parenchyma before and after vagotomy. There is evidence of a profound cardiopulmonary reflex that produces systemic hypotension, bradycardia, and decreased RSNA, in addition to stimulated respiratory drive (26). The observed depressor effects may derive from withdrawal of sympathetic efferent activity.…”

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confidence: 99%

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Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

Wang¹,

Soukhova²,

Proctor³

et al. 2003

Journal of Applied Physiology

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causes hypotension by activating pulmonary sympathetic afferents in the rabbit. J Appl Physiol 95: 233-240, 2003. First published April 4, 2003 10.1152/japplphysiol.00584.2002 activates sympathetic afferents in the heart, intestine, and kidney, and it alters hemodynamics. However, we know little about the influence of pulmonary sympathetic afferents on circulation. Activation of pulmonary afferents by directly injecting stimulants into the lung parenchyma permits examination of reflexes that originate in the lung without confounding effects from the systemic circulation. In the present study, we tested the hypothesis that pulmonary sympathetic afferents exert a significant influence on hemodynamics. We examined reflex effects of injecting BK (1 g/kg in 0.1 ml) into the lung parenchyma on circulation in anesthetized, open-chest, artificially ventilated rabbits. BK significantly decreased mean arterial blood pressure (BP) (27 Ϯ 3 mmHg) and heart rate (19 Ϯ 4 beats/min). Both effects remained after bilateral vagotomy. To rule out possible direct systemic vasodilation by BK, we examined renal sympathetic nerve activity (RSNA) in response to BK injection and examined BP responses to injection of ACh (0.1 ml of 10 Ϫ4 M). BK suppressed the RSNA before and after vagotomy. ACh did not change BP when injected into the lung parenchyma, but it decreased BP (31 Ϯ 3 mmHg) when injected into the right atrium. Our data indicate that activating pulmonary sympathetic afferents reflexly suppresses hemodynamics. lung receptors; lung reflex; depressor effect; bradycardia FOR DECADES IT HAS BEEN RECOGNIZED that cardiovascular regulation is strongly influenced by inputs from the lung (24). These pulmonary inputs are believed to travel mainly in the vagus nerves. Mechanically activating pulmonary stretch receptors (33) or chemically activating pulmonary C fibers (4) in the vagus nerve can cause peripheral vasodilation and changes in heart rate. Activation of some pulmonary vagal afferents in the rabbit causes a slight pressor response in addition to stimulating breathing (25, 34). However, information regarding the reflex effects evoked from pulmonary sympathetic afferents is scarce and debatable (23).Sensory information in the lung is transmitted through vagal and sympathetic nerves (32). Morphological evidence points to the existence of sympathetic afferents in the lungs (13,18,22). Pulmonary sympathetic afferent activity has been recorded in stellate ganglia (9) and white rami of T 2

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Section: Discussionsupporting

confidence: 53%

“…2). Reflex effects on respiratory drive occurred in most but not all cases (26). Reflex hemodynamic effects showed a depressor response in 38 of 59 trials on 18 rabbits (64%).…”

Section: Resultsmentioning

confidence: 93%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

Wang¹,

Soukhova²,

Proctor³

et al. 2003

Journal of Applied Physiology

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Sensory Nerves in Lung and Airways

Lee

2014

Comprehensive Physiology

110

156

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Sensory nerves innervating the lung and airways play an important role in regulating various cardiopulmonary functions and maintaining homeostasis under both healthy and disease conditions. Their activities conducted by both vagal and sympathetic afferents are also responsible for eliciting important defense reflexes that protect the lung and body from potential health-hazardous effects of airborne particulates and chemical irritants. This article reviews the morphology, transduction properties, reflex functions, and respiratory sensations of these receptors, focusing primarily on recent findings derived from using new technologies such as neural immunochemistry, isolated airway-nerve preparation, cultured airway neurons, patch-clamp electrophysiology, transgenic mice, and other cellular and molecular approaches. Studies of the signal transduction of mechanosensitive afferents have revealed a new concept of sensory unit and cellular mechanism of activation, and identified additional types of sensory receptors in the lung. Chemosensitive properties of these lung afferents are further characterized by the expression of specific ligand-gated ion channels on nerve terminals, ganglion origin, and responses to the action of various inflammatory cells, mediators, and cytokines during acute and chronic airway inflammation and injuries. Increasing interest and extensive investigations have been focused on uncovering the mechanisms underlying hypersensitivity of these airway afferents, and their role in the manifestation of various symptoms under pathophysiological conditions. Several important and challenging questions regarding these sensory nerves are discussed. Searching for these answers will be a critical step in developing the translational research and effective treatments of airway diseases.

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Morphologically Identified Sensory Receptor End-Organs in the Airways, Lungs and Visceral Pleura

Brouns

Pintelon

Timmermans

et al. 2011

Novel Insights in the Neurochemistry and Function of Pulmonary Sensory Receptors

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Bradykinin stimulates respiratory drive by activating pulmonary sympathetic afferents in the rabbit

Cited by 20 publications

References 32 publications

Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

Sensory Nerves in Lung and Airways

Morphologically Identified Sensory Receptor End-Organs in the Airways, Lungs and Visceral Pleura

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