Tenidap, a novel anti-inflammatory agent, is an opener of the inwardly rectifying K + channel hKir2.3
European Journal of Pharmacology, ISSN: 0014-2999, Vol: 435, Issue: 2, Page: 153-160
2002
- 24Citations
- 18Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations24
- Citation Indexes24
- 24
- CrossRef14
- Captures18
- Readers18
- 18
Article Description
We studied the effect of a novel anti-inflammatory agent, tenidap, on a cloned inwardly rectifying K + channel, hKir2.3. Tenidap (a) potently potentiated 86 Rb + efflux through hKir2.3 channels expressed in Chinese hamster ovary cells (EC 50 =402 nM), (b) reversibly and dose-dependently increased whole-cell and macro-patch hKir2.3 currents (maximum whole-cell current response to tenidap was 230±27% of control; EC 50 =1.3 μM.), and (c) caused dose-dependent and Ba 2+ -sensitive membrane hyperpolarizations and concurrent decreases in input resistance. Potentiation of hKir2.3 by tenidap was unaffected by inhibitors of phospholipase A 2, protein kinase C, or arachidonic acid metabolic pathways. The action of tenidap was not intracellular. Tenidap also had little or no effect on currents flowing through hKir2.1, Kv1.5, and μ1 Na + channels. Our results demonstrate that tenidap is a potent opener of hKir2.3 and suggest that it can serve as a valuable pharmacological tool for studying physiological and pathological processes involving Kir2.3.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0014299901015904; http://dx.doi.org/10.1016/s0014-2999(01)01590-4; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0037169255&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11821021; https://linkinghub.elsevier.com/retrieve/pii/S0014299901015904; http://linkinghub.elsevier.com/retrieve/pii/S0014299901015904; http://api.elsevier.com/content/article/PII:S0014299901015904?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:S0014299901015904?httpAccept=text/plain; http://dx.doi.org/10.1016/s0014-2999%2801%2901590-4; https://dx.doi.org/10.1016/s0014-2999%2801%2901590-4
Elsevier BV
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