2003
DOI: 10.1165/rcmb.2002-0104oc
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Effects of Endothelin-1 on Epithelial Ion Transport in Human Airways

Abstract: Endothelin-1 (ET-1) exerts many biological effects in airways, including bronchoconstriction, airway mucus secretion, cell proliferation, and inflammation. We investigated the effect of ET-1 on Na absorption and Cl secretion in human bronchial epithelial cells. Addition of 10(-7) M ET-1 had no effect on the inhibition of the short circuit current (Isc) induced by amiloride, a Na channel blocker. Addition of 10(-7) M ET-1 to the apical bath in the presence of amiloride increased Isc in cultured human bronchial … Show more

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Cited by 22 publications
(12 citation statements)
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“…Although VX-770 had some effect on unstimulated HBE, likely because of endogenous levels of cAMP in these cells (47), the maximal pharmacological effect of VX-770 on ion and fluid transport required stimulation of the cAMP/PKA signaling pathway by either forskolin or VIP. It is likely that the situation is more dynamic in vivo, where neuronal pathways and mechanical forces exerted on the airway regulate the epithelial cellular signaling pathways to control the activity of CFTR and other ion transport pathways to regulate fluid transport (48,49).…”
Section: Discussionmentioning
confidence: 98%
“…Although VX-770 had some effect on unstimulated HBE, likely because of endogenous levels of cAMP in these cells (47), the maximal pharmacological effect of VX-770 on ion and fluid transport required stimulation of the cAMP/PKA signaling pathway by either forskolin or VIP. It is likely that the situation is more dynamic in vivo, where neuronal pathways and mechanical forces exerted on the airway regulate the epithelial cellular signaling pathways to control the activity of CFTR and other ion transport pathways to regulate fluid transport (48,49).…”
Section: Discussionmentioning
confidence: 98%
“…The proliferative response to ET-1 (10 )7 M) was significantly inhibited by BQ-123 (10 )6 M), an ET A antagonist, and TAK044 (10 )6 M), an ET A /ET B antagonist, but not by BQ-788 (10 )6 M), an ET B antagonist, suggesting that the ET-1stimulated proliferation was mediated via ET A receptors, as shown in Figure 5. The dose of antagonists were within the common limits [25,26].…”
Section: Effects Of Et Receptor Antagonists On Proliferative Responsementioning
confidence: 92%
“…Its activity contributes to the maintenance of endogenous vasomotor tone by producing a long-lasting vasoconstriction of the underlying smooth muscle cells 24. In addition, ET-1 is also produced by smooth muscle cells,25 cardiomyocites,26 leukocytes,26 macrophages,27 mesangial cells,28,29 airway epithelium,3032 and alveolar epithelial cells (AECs) 33,34. ET-1 is released during various injurious stimuli, including shear stress, thrombin, angiotensin II, cytokines, and free radicals, whereas atrial natriuretic peptide, prostacyclin, and NO inhibit its synthesis and release 35,36…”
Section: Endothelin Systemmentioning
confidence: 99%