Novel Antitussive Effect of Suplatast Tosilate in Guinea Pigs

Zhou, Jian-Rong; Syono, Ryo Ichi; Fukumi, Syu Ichi; Kimoto, Kenji; Shirasaki, Tetsuya; Soeda, Fumio; Takahama, Kazuo

doi:10.1159/000369977

Cited by 3 publications

(3 citation statements)

References 16 publications

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“…In addition, we have reported that a cough induced by the mechanical stimulation of tracheal bifurcation is resistant to treatment by codeine (41). Our own preliminary study showed that suplatast inhibits this codeine-resistant cough (49). Interestingly, ophiopogonin-D, an active component of Bakumondo-to, which is a Chinese herbal medicine and is effective for intractable coughs, also inhibits the excitability of paratracheal ganglia neurons, although inhibition mechanisms are different between the two substances.…”

Section: L776mentioning

confidence: 96%

Effects of suplatast tosilate on acutely dissociated sensory and paratracheal ganglia neurons

Zhou

Shirasaki

Soeda

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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In this study, we investigated the effects of suplatast on acutely dissociated single neurons of sensory and paratracheal ganglia using a patch-clamp technique. Suplatast had little effect on various responses caused by capsaicin, acid, bradykinin, serotonin and adenosine 5'-triphosphate in rat sensory neurons. Suplatast, even at 10-3 M, also did not induce any current at various membrane potentials in rat and guinea pig paratracheal ganglia neurons. Further, acetylcholine- and bradykinin-induced depolarizations were not affected by suplatast. On the other hand, in rat paratracheal ganglia neurons, 10-5 M nicotine-induced current were inhibited by suplatast in a concentration-dependent manner with a 50% inhibitory concentration of 9.86x10-5 M. The effect was noncompetitive and voltage-dependent. Furthermore, the effect was use-independent and not affected by the pretreatment time of suplatast. The results suggested that suplatast may inhibit neurotransmission at the paratracheal ganglia via the inhibition of nicotinic current. Thus, suplatast may attenuate cough production through the improvement of pathological conditions of the lower airway via suppressed acetylcholine release from the postganglionic nerve terminal.

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Section: L776mentioning

confidence: 96%

Effects of suplatast tosilate on acutely dissociated sensory and paratracheal ganglia neurons

Zhou

Shirasaki

Soeda

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…But the codeine-resistant cough was reduced by H 1 antagonists (our unpublished data). Interestingly, suplatast also inhibits this codeine-resistant cough [11]. Therefore, suplatast might be also effective for treating atopic cough.…”

Section: Resultsmentioning

confidence: 99%

“…Previously, we found that suplatast inhibits codeine-resistant coughs in guinea pigs with bronchitis or treated with an angiotensin-converting enzyme inhibitor [11]. However, the antitussive effect of suplatast does not appear to be due to the anti-allergic effect caused by Th2 cytokine inhibition.…”

Section: Introductionmentioning

confidence: 98%

Direct Potentiation of Capsaicin Current by Histamine and Its Effect by Suplatast on Rat Trigeminal Ganglia Neurons

et al. 2018

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In this study, we investigated the effect of histamine on capsaicin-induced current and its influence by suplatast in rat trigeminal ganglia neurons using a patch-clamp technique. We found that histamine directly potentiated capsaicin-induced currents in rat sensory neurons, and suplatast had little effect on this potentiation. Since it has been known that suplatast suppresses histamine release from mast cells, it is possible that suplatast inhibits the activation of nociceptive fibers in the pathological condition via prevention of histamine-induced potentiation of the transient receptor potential vanilloid 1 receptor-mediated currents.

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Polygenic risk score for ACE-inhibitor-associated cough based on the discovery of new genetic loci

Ghouse

Tragante

Muhammad

et al. 2022

European Heart Journal

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Aims To search for sequence variants associated with ACEi discontinuation and to test their association with ACEi-associated adverse drug reactions (ADRs). Methods and results A genome-wide association study (GWAS) on ACEi discontinuation was conducted, including 33 959 ACEi-discontinuers and 44 041 controls. Cases were defined as persons who switched from an ACEi treatment to an angiotensin receptor blocker. Controls were defined as persons who continued ACEi treatment for at least 1 year. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were computed for ACEi discontinuation risk by mixed model regression analysis. Summary statistics from the individual cohorts were meta-analyzed with a fixed-effects model. To test for association with specific ACEi-associated ADRs, any genome-wide significant (P < 5 × 10-8) ACEi discontinuation variants was tested for association with ACEi-associated cough and angioedema. A polygenetic risk score (PRS) based on ACEi discontinuation GWAS data was constructed and tested for association with ACEi-associated cough and angioedema in two population-based samples. In total, seven genetic genome-wide loci were identified, of which six were previously unreported. The strongest association with ACEi discontinuation was at 20q13.3 (NTSR1; OR: 1.21; 95% CI: 1.17–1.24; P = 2.1 × 10–34). Five of seven lead variants were associated with ACEi-associated cough, whereas none were associated with ACEi-associated angioedema. The ACEi discontinuation PRS was associated with ACEi-associated cough in a dose–response manner but not with ACEi-associated angioedema. ACEi discontinuation was genetically correlated with important causes for cough, including gastro-esophageal reflux disease, allergic rhinitis, hay fever, and asthma, which indicates partly shared genetic underpinning between these traits. Conclusion This study showed the advantage of using prescription patterns to discover genetic links with ADRs. In total, seven genetic loci that associated with ACEi discontinuation were identified. There was evidence of a strong association between our ADR phenotype and ACEi-associated cough. Taken together, these findings increase insight into the pathophysiological processes that underlie ACEi-associated ADRs.

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Novel Antitussive Effect of Suplatast Tosilate in Guinea Pigs

Cited by 3 publications

References 16 publications

Effects of suplatast tosilate on acutely dissociated sensory and paratracheal ganglia neurons

Effects of suplatast tosilate on acutely dissociated sensory and paratracheal ganglia neurons

Direct Potentiation of Capsaicin Current by Histamine and Its Effect by Suplatast on Rat Trigeminal Ganglia Neurons

Polygenic risk score for ACE-inhibitor-associated cough based on the discovery of new genetic loci

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