Cough induced by stimulation of capsaicin‐sensitive sensory neurons in conscious guinea‐pigs

Forsberg, K.; Karlsson, J.‐A.

doi:10.1111/j.1748-1716.1986.tb07981.x

Cited by 100 publications

(48 citation statements)

References 6 publications

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“…However caution should be used in comparing antitussive effects of drugs on cough elicited by different irritant stimuli, such as citric acid and capsaicin. Although previous investigators have suggested that citric acid and capsaicin act by the same mechanism on the basis of neuropeptide depletion experiments using capsaicin (Forsberg & Karlsson, 1986), we have recently shown that citric acid can elicit cough by the same or different mechanisms as capsaicin depending upon the dose of citric acid administered (Bolser et al, 1991a). These observations underscore the importance of using the same tussigenic stimulus when comparing activities of antitussive drugs.…”

Section: Discussionmentioning

confidence: 99%

“…It was not known whether this action was due to an effect of GABAA or GABAB receptor stimulation. However, there is good evidence that GABAB receptors inhibit the activity of peripheral sensory afferents (Green & Cottrell, 1988) such as pulmonary C-fibres (Belvisi et al, 1989) that may influence the production of cough (Forsberg & Karlsson, 1986). Therefore, we speculated that GABAB agonists would have antitussive activity and we studied this phenomenon in several animal models of cough.…”

Section: Introductionmentioning

confidence: 99%

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Antitussive effects of GABA_B agonists in the cat and guinea‐pig

Bolser¹,

Aziz²,

DeGennaro³

et al. 1993

British J Pharmacology

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1 GABAB agonists inhibit neuronal processes which are important in the pathogenesis of airway disease, such as bronchospasm. Cough is a prominent symptom of pulmonary disease, but the effects of GABAB agonists on this airway reflex are unknown. Experiments were conducted to determine the antitussive effect of GABAB receptor agonists in comparison to the known antitussive agents, codeine and dextromethorphan. 2 Unanaesthetized guinea-pigs were exposed to aerosols of 0.3 mM capsaicin to elicit coughing, which was detected with a microphone and counted. Cough also was produced in anaesthetized cats by mechanical stimulation of the intrathoracic trachea and was recorded from electromyograms of respiratory muscle activity. 3 In guinea-pigs, the GABAB agonists baclofen and 3-aminopropyl-phosphinic acid (3-APPi) produced dose-dependent inhibition of capsaicin-induced cough when administered by subcutaneous or inhaled routes. The potencies of baclofen and 3-APPi compared favourably with codeine and dextromethorphan.4 The GABAB antagonist, CGP 35348 (0.3-30mg kg-', s.c.) inhibited the antitussive effect of baclofen (3.0mgkg-', s.c.). However, CGP 35348 (10mgkg-', s.c.) had no effect on the antitussive activity of codeine (30mgkg-', s.c.). The antitussive effect of baclofen was not influenced by the GABAA antagonist, bicuculline (3mgkg-', s.c.) or naloxone (0.3mgkg'1, s.c.). 5 In the cat, baclofen (0.3-3.0 mg kg-', i.v.) decreased mechanically-induced cough in a dosedependent manner. In this model, baclofen (ED_0 = 0.63 mg kg-l) was less potent than either codeine or dextromethorphan. The antitussive effect of baclofen in the cat was antagonized by the GABAB antagonists, CGP 35348 (10 mg kg', i.v.) and 3-aminopropylphosphonic acid (3 mg kg', i.v.). 6 We show that baclofen and 3-APPi have antitussive effects in the guinea-pig and cat and these effects are mediated by GABAB receptors.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antitussive effects of GABA_B agonists in the cat and guinea‐pig

Bolser¹,

Aziz²,

DeGennaro³

et al. 1993

British J Pharmacology

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“…Furthermore, a larger contribution of airway C-fibers on the airway contraction was observed in BHS compared with BHR in a preliminary experiment. It is known that citric acid-induced cough is produced by the effect of citric acid on capsaicin-sensitive sensory neurons [6,7], while the bronchoconstriction induced by citric acid in guinea pigs involves a muscarinic mechanism [2,6]. It is, therefore, interesting to investigate the relationship between cough occurrence and airway sensitivity in these model animals with different muscarinic functions and the role of C-fibers in the airway.…”

Section: Discussionmentioning

confidence: 99%

The Difference in Citric Acid-Induced Cough in Congenitally Bronchial-Hypersensitive (BHS) and Bronchial-Hyposensitive (BHR) Guinea Pigs.

et al. 2001

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Cough elicitation and major physiological factors influencing cough occurrence were investigated in congenitally bronchial-hypersensitive (BHS) and -hyposensitive (BHR) guinea pigs exposed to citric acid (0.3 M) aerosol for 10 min. The number of cough in BHS was significantly larger than in BHR, while the latency to cough in BHS was significantly shorter than in BHR. Pretreatment with atropine (0.2%), lidocaine (2%) or salbutamol (0.1%) aerosol and desensitization of C-fibers with capsaicin (100 mg/kg) decreased the cough numbers in both BHS and BHR. The salbutamol, atropine and capsaicin pretreatments prolonged the cough latency in BHS, but only salbutamol prolonged the latency in BHR. After salbutamol pretreatment all BHR guinea pigs exhibited cough, while 66.7% of BHS guinea pigs exhibited it. Vagal blocking by atropine suppressed coughing in both BHS and BHR. Only a small number (33.3%) of BHR guinea pigs and no BHR guinea pigs exhibited a cough response after capsaicin and lidocaine pretreatment whereas many BHS guinea pigs still produced cough after such pretreatment. The present study demonstrated that the cough responsiveness to citric acid aerosol was significantly higher in BHS than in BHR. It was revealed that airway smooth muscle contraction and functional and/or morphological development of airway nervous receptors, especially C-fiber endings, contributed to aggravation of coughing in BHS.

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“…After overnight fasting with water ad libitum, the guinea-pigs were randomly assigned to the experimental groups (n = 10 for each dose) and orally pretreated with vehicle (controls), moguisteine (7.5, 15 and 30 mg kg-') or codeine (10, 20 and 40 mg kg-') 1 h before exposure for 5 min to a 30 AM capsaicin aerosol (Forsberg & Karlsson, 1986). The aerosol characteristics and the cough counting were as previously described; in control animals capsaicin induced 7-12 coughs.…”

Section: Methodsmentioning

confidence: 99%