The rapidly adapting receptors in mammalian airways and their responses to changes in extravascular fluid volume

Kappagoda, C. T.; Ravindran, Krishnan

doi:10.1113/expphysiol.2006.033209

Cited by 23 publications

(13 citation statements)

References 42 publications

(63 reference statements)

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“…Brief periods of apnea elicit marked increases in MSNA (38). Rapidly adapting vagal sensory receptors located in the airways respond to lung inflation and deflation, and also to increases in left atrial pressure and extravascular pulmonary fluid volume (57). Peripheral chemoreceptor reflexes.…”

Section: Afferent Mechanismsmentioning

confidence: 99%

Sympathetic Nervous System Activation in Human Heart Failure

Floras

2009

Journal of the American College of Cardiology

467

366

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Disturbances in cardiovascular neural regulation, influencing both disease course and survival, progress as heart failure worsens. Heart failure due to left ventricular systolic dysfunction has long been considered a state of generalized sympathetic activation, itself a reflex response to alterations in cardiac and peripheral hemodynamics that is initially appropriate, but ultimately pathological. Because arterial baroreceptor reflex vagal control of heart rate is impaired early in heart failure, a parallel reduction in its reflex buffering of sympathetic outflow has been assumed. However, it is now recognized that: 1) the time course and magnitude of sympathetic activation are target organ-specific, not generalized, and independent of ventricular systolic function; and 2) human heart failure is characterized by rapidly responsive arterial baroreflex regulation of muscle sympathetic nerve activity (MSNA), attenuated cardiopulmonary reflex modulation of MSNA, a cardiac sympathoexcitatory reflex related to increased cardiopulmonary filling pressure, and by individual variation in nonbaroreflex-mediated sympathoexcitatory mechanisms, including coexisting sleep apnea, myocardial ischemia, obesity, and reflexes from exercising muscle. Thus, sympathetic activation in the setting of impaired systolic function reflects the net balance and interaction between appropriate reflex compensatory responses to impaired systolic function and excitatory stimuli that elicit adrenergic responses in excess of homeostatic requirements. Recent observations have been incorporated into an updated model of cardiovascular neural regulation in chronic heart failure due to ventricular systolic dysfunction, with implications for the clinical evaluation of patients, application of current treatment, and development of new therapies.

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Section: Afferent Mechanismsmentioning

confidence: 99%

Sympathetic Nervous System Activation in Human Heart Failure

Floras

2009

Journal of the American College of Cardiology

467

366

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“…RARs are myelinated fibers located in the larynx, trachea, and bronchi [47]. Similar to C-nerve fibers, activation of RARs leads to bronchoconstriction, cough, and increased mucus secretion [48].…”

Section: Airway Receptorsmentioning

confidence: 99%

Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure

2014

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The body responds to environmental stressors by triggering autonomic reflexes in the pulmonary receptors, baroreceptors, and chemoreceptors to maintain homeostasis. Numerous studies have shown that exposure to various gases and airborne particles can alter the functional outcome of these reflexes, particularly with respect to the cardiovascular system. Modulation of autonomic neural input to the heart and vasculature following direct activation of sensory nerves in the respiratory system, elicitation of oxidative stress and inflammation, or through other mechanisms is one of the primary ways that exposure to air pollution affects normal cardiovascular function. Any homeostatic process that utilizes the autonomic nervous system to regulate organ function might be affected. Thus, air pollution and other inhaled environmental irritants have the potential to alter both local airway function and baro-and chemoreflex responses, which modulate autonomic control of blood pressure and detect concentrations of key gases in the body. While each of these reflex pathways causes distinct responses, the systems are heavily integrated and communicate through overlapping regions of the brainstem to cause global effects. This short review summarizes the function of major pulmonary sensory receptors, baroreceptors, and carotid body chemoreceptors and discusses the impacts of air pollution exposure on these systems.

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“…Cardiovascular disorders such as hypertension, chronic heart failure, ischaemic heart disease and arrhythmia are the most frequent disorders seen in patients with COPD [9,[34][35][36]. In the natural course of these cardiovascular chronic diseases occur acute events, which may result in respiratory symptoms [21,23,24] (Fig. 3).…”

Section: Cardiovascular Disordersmentioning

confidence: 99%

Mechanisms of acute exacerbation of respiratory symptoms in chronic obstructive pulmonary disease

Roca

Verduri

Corbetta

et al. 2013

Eur J Clin Investigation

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Exacerbations of chronic obstructive respiratory disease (ECOPD) are acute events characterized by worsening of the patient's respiratory symptoms, particularly dyspnoea, leading to change in medical treatment and/or hospitalisation. AECOP are considered respiratory diseases, with reference to the respiratory nature of symptoms and to the involvement of airways and lung. Indeed respiratory infections and/or air pollution are the main causes of ECOPD. They cause an acute inflammation of the airways and the lung on top of the chronic inflammation that is associated with COPD. This acute inflammation is responsible of the development of acute respiratory symptoms (in these cases the term ECOPD is appropriate). However, the acute inflammation caused by infections/pollutants is almost associated with systemic inflammation, that may cause acute respiratory symptoms through decompensation of concomitant chronic diseases (eg acute heart failure, thromboembolism, etc) almost invariably associated with COPD. Most concomitant chronic diseases share with COPD not only the underlying chronic inflammation of the target organs (i.e. lungs, myocardium, vessels, adipose tissue), but also clinical manifestations like fatigue and dyspnoea. For this reason, in patients with multimorbidity (eg COPD with chronic heart failure and hypertension, etc), the exacerbation of respiratory symptoms may be particularly difficult to investigate, as it may be caused by exacerbation of COPD and/or ! comorbidity, (e.g. decompensated heart failure, arrhythmias, thromboembolisms) without necessarily involving the airways and lung. In these cases the term ECOPD is inappropriate and misleading.

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The rapidly adapting receptors in mammalian airways and their responses to changes in extravascular fluid volume

Cited by 23 publications

References 42 publications

Sympathetic Nervous System Activation in Human Heart Failure

Sympathetic Nervous System Activation in Human Heart Failure

Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure

Mechanisms of acute exacerbation of respiratory symptoms in chronic obstructive pulmonary disease

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