Document Detail


Acid-sensitive vagal sensory pathways and cough.
MedLine Citation:
PMID:  17289409     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acid is an important mediator in the pathogenesis of cough. Inhalation of exogenous acid triggers cough and endogenous acid may contribute to cough in respiratory diseases. Acid directly stimulates vagal bronchopulmonary sensory nerves that regulate the cough reflex. Consistent with their putative role in defence against aspiration and inhaled irritants, Adelta-fibre nociceptors in the large airways are most efficiently stimulated by rapid acidification. In contrast, acid-sensitive properties of the C-fibre nociceptors allow for continuous monitoring of pH which is likely important in inflammation. Acid is also the single most important mediator in the pathogenesis of cough due to gastro-oesophageal reflux (GOR). The cough pathways can be sensitized by the sensory inputs from the oesophagus. This sensitization is likely mediated by a subset of the vagal oesophageal sensory nerves distinguished by discriminative responsiveness to noxious stimuli (nociceptors). The receptors underlying acid sensitivity of vagal sensory nerves are incompletely understood. The role of TRPV1 has been established but the roles of acid-sensing ion channels (ASIC) and other receptors await more definitive investigation. Here, we provide a brief overview of the cough-related acid-sensitive sensory pathways and discuss the mechanisms of acid sensitivity.
Authors:
Marian Kollarik; Fei Ru; Bradley J Undem
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Publication Detail:
Type:  Journal Article; Review     Date:  2006-12-13
Journal Detail:
Title:  Pulmonary pharmacology & therapeutics     Volume:  20     ISSN:  1094-5539     ISO Abbreviation:  Pulm Pharmacol Ther     Publication Date:  2007  
Date Detail:
Created Date:  2007-04-09     Completed Date:  2007-06-26     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  9715279     Medline TA:  Pulm Pharmacol Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  402-11     Citation Subset:  IM    
Affiliation:
The Johns Hopkins School of Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, MD 21224, USA. kollarik@jhmi.edu
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MeSH Terms
Descriptor/Qualifier:
Acids / adverse effects*
Afferent Pathways / physiology
Animals
Cough / physiopathology*
Gastroesophageal Reflux / complications,  physiopathology
Humans
Hydrogen-Ion Concentration
Ion Channels / physiology
Reflex / physiology
Respiratory System / innervation*
Respiratory Tract Diseases / physiopathology
Sensory Receptor Cells / physiology
Vagus Nerve / physiology*
Grant Support
ID/Acronym/Agency:
R01 DK074480-01A1/DK/NIDDK NIH HHS; R01 HL038095-18/HL/NHLBI NIH HHS; R01 HL062296-08/HL/NHLBI NIH HHS; R01 HL062296-12/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Acids; 0/Ion Channels
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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