ArticleBritish journal of pharmacology2005
Vasotocin and vasopressin stimulation of the chloride secretion in the human bronchial epithelial cell line, 16HBE14o-.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 122 citations in OpenAlex.
- Chiral Monoamidines as Effective Organocatalysts for the Stereoselective Synthesis of Oxindoles under Homogeneous and Heterogeneous Conditions.The Journal of organic chemistry · 2025Article
- Dopamine, norepinephrine, and vasopressin accelerate particle transport velocity in murine tracheal epithelium via substance-specific receptor pathways: dependency on intra- and extracellular CaFrontiers in pharmacology · 2024Article
- A [3 + 2] cycloaddition/C-arylation of isatinRSC advances · 2020Article
- Organocatalytic asymmetric allylic amination of Morita-Baylis-Hillman carbonates of isatins.Beilstein journal of organic chemistry · 2012Article
- Protein processing and inflammatory signaling in Cystic Fibrosis: challenges and therapeutic strategies.Current molecular medicine · 2010Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Effects of neuropeptides of the vasopressin family on Cl(-) secretion have not yet been reported in lung. Using the 16HBE14o- bronchial epithelial cell line, we investigated their action on Cl(-) secretion. 2. In symmetrical Cl(-) solutions, basolateral application of arginine vasotocin (AVT), oxytocin or isotocin induced a transient I(sc) stimulation (I(peak)), whereas arginine vasopressin (AVP) did not. The effects of different Cl(-) channel blockers and of a protein kinase C (PKC) inhibitor suggest that CFTR is involved in I(peak). The calcium-activated K(+) channel (SK4) and the Cl(-)/HCO(-)(3) exchanger favor the driving force for AVT-mediated Cl(-) secretion. The antagonists of V1a (SR49059)- and V1b (SSR149415)-receptors blocked I(peak), while SR121463B, a V2 receptor antagonist, did not. These results point to the stimulation of a V1-like receptor mediating I(peak) and presenting an efficacy order, AVT>oxytocin>isotocin>>AVP. 3. When a serosal to mucosal Cl(-) gradient was applied, AVT and AVP both stimulated I(sc) according to a biphasic profile, I(peak) being followed by a plateau phase (I(plateau)). The pharmacology of I(plateau) suggests that CFTR channels are involved and that Na(+)/K(+)/2Cl(-) is the only transporter associated with I(plateau). dDAVP, a V2 receptor agonist-induced I(plateau) with the same potency as AVP, suggesting the involvement of V2 receptors in the AVP-induced I(plateau). V2 receptors are present on both opposite membranes, while V1-like receptors are mainly expressed on the basolateral membranes. RT-PCR experiments show the expression of V1a, V1b, V2 and vasopressin-activated calcium-mobilizing (VACM) receptors mRNAs.
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