Bradykinin–evoked sensitization of airway sensory nerves: A mechanism for ACE–inhibitor cough

@article{Fox1996BradykininevokedSO,
  title={Bradykinin–evoked sensitization of airway sensory nerves: A mechanism for ACE–inhibitor cough},
  author={Alyson J. Fox and Umesh Lalloo and Maria G. Belvisi and Micaela Maria Bernareggi and Kian Fan Chung and Peter John Barnes},
  journal={Nature Medicine},
  year={1996},
  volume={2},
  pages={814-817}
}
Cough accompanied by an increased sensitivity of the cough reflex is the most common symptom of inflammatory airway disease1,5. This symptom is also frequently reported in patients receiving angiotensin–converting enzyme (ACE) inhibitors as therapy for heart failure or hypertension2–4, although the underlying mechanism is unknown. We have investigated the possibility that the inflammatory peptide bradykinin, normally degraded by ACE, causes sensitization of airway sensory nerves and an… Expand
Augmentation of spontaneous cough by enalapril through up-regulation of bradykinin B1 receptors in guinea pigs.
TLDR
The present results indicate that enalapril-induced cough is mediated by up-regulation of bradykinin B(1) receptors. Expand
Pharmacology of Bradykinin-Evoked Coughing in Guinea Pigs
TLDR
The data suggest that bradykinin induces coughing in guinea pigs by activating B2 receptors on bronchopulmonary C-fibers, and it is speculated that therapeutics targeting the actions of bradykinsin may prove useful in the treatment of cough. Expand
Role of bradykinin and tachykinins in the potentiation by enalapril of coughing induced by citric acid in pigs
TLDR
Data suggest that ACE‐inhibitor‐induced enhancement of the cough reflex is mainly due to tachykinins and not to bradykinin in the authors' pig model, suggesting that Bradykinin plays a major role in coughing induced by citric acid alone. Expand
TRPV1 as a cough sensor and its temperature-sensitive properties.
TLDR
In the respiratory tract, TRPV1, a non-selective cation channel and a polymodal transducer, is expressed primarily in non-myelinated sensory nerves, which play an important role in regulating the physiological function of the TRpV1-expressing airway sensory nerves and the sensitivity of their reflex responses, such as cough. Expand
Interaction of noscapine with the bradykinin mediation of the cough response.
TLDR
Noscapine is shown to be a non-competitive inhibitor of bradykinin in guinea pig ileum and it is possible that noscapine suppresses cough by blocking the effect of bradaykinin receptor activation in the airways. Expand
Protease-activated receptor-2 activation exaggerates TRPV1-mediated cough in guinea pigs.
TLDR
Par2 activation, by sensitizing TRPV1 in primary sensory neurons, may play a role in the exaggerated cough observed in certain airways inflammatory diseases such as asthma and chronic obstructive pulmonary disease. Expand
Bradykinin‐evoked sensitization of neuropeptide release from afferent neurons in the guinea‐pig lung
TLDR
The results suggest that BK‐induced stimulation of prostaglandin synthesis results in facilitation of histamine–evoked release of pro‐inflammatory neuropeptides from afferent neurons, a mechanism that probably becomes relevant during inflammation, and that can be blocked by a bradykinin B2 receptor antagonist. Expand
Mechanistic studies of acid-evoked coughing in anesthetized guinea pigs.
TLDR
The mechanisms of citric acid-evoked coughing in anesthetized guinea pigs are characterized and data indicate that coughing evoked by acid is mediated by direct activation of capsaicin-insensitive vagal afferent nerves, perhaps through sequential activation of acid-sensing ion channels and chloride channels. Expand
Prostaglandin E2 sensitizes the cough reflex centrally via EP3 receptor-dependent activation of NaV 1.8 channels
TLDR
Results indicate that PGE2 plays an important role in central sensitization of the cough reflex and suggest that central EP3 receptors and/or NaVv 1.8 channels may represent novel antitussive molecular targets. Expand
Bradykinin sensitizes the cough reflex via a B2 receptor dependent activation of TRPV1 and TRPA1 channels through metabolites of cyclooxygenase and 12-lipoxygenase
TLDR
Findings show that central BK administration sensitizes cough and enhances airway obstruction via a B2 receptor/TRPV1 and/or TRPA1 channels which are coupled via metabolites of COX and/ or 12-LOX enzymes. Expand
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