pubmed-article:9676733 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0028778 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0000477 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
pubmed-article:9676733 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:9676733 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:9676733 | pubmed:dateCreated | 1998-10-1 | lld:pubmed |
pubmed-article:9676733 | pubmed:abstractText | The effects of 4-aminopyridine (4-AP) on the transient outward current (I(to)) were investigated in rat ventricular cardiomyocytes at different values of intracellular pH (pHi) and extracellular pH (pHo). The 4-AP was administered either extracellularly (bath application) or intracellularly (diffusion from the intrapipette solution). The 4-AP diminished I(to) given either from inside or outside the cell membrane. The block by extracellularly applied 4-AP (4-APo) of the peak amplitude of I(to) was decreased by external acidification but increased by external alkalinization; conversely, the block by 4-APo was decreased by internal alkalinization but increased by internal acidification. Intracellularly applied 4-AP (3 mM) was more effective at low pHi. Because 4-AP is a tertiary amine and exists in protonated and unprotonated forms, these results are in agreement with the assumption that one major mechanism for 4-AP to block I(to) is to penetrate the cell membrane in its uncharged form and to reach intracellular binding sites in its protonated form. | lld:pubmed |
pubmed-article:9676733 | pubmed:language | eng | lld:pubmed |
pubmed-article:9676733 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9676733 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9676733 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9676733 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9676733 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9676733 | pubmed:month | Jul | lld:pubmed |
pubmed-article:9676733 | pubmed:issn | 0160-2446 | lld:pubmed |
pubmed-article:9676733 | pubmed:author | pubmed-author:SampsonS RSR | lld:pubmed |
pubmed-article:9676733 | pubmed:author | pubmed-author:NawrathHH | lld:pubmed |
pubmed-article:9676733 | pubmed:author | pubmed-author:WegenerJ WJW | lld:pubmed |
pubmed-article:9676733 | pubmed:author | pubmed-author:PeiterAA | lld:pubmed |
pubmed-article:9676733 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9676733 | pubmed:volume | 32 | lld:pubmed |
pubmed-article:9676733 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9676733 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9676733 | pubmed:pagination | 134-8 | lld:pubmed |
pubmed-article:9676733 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:9676733 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9676733 | pubmed:articleTitle | Mechanism of block by 4-aminopyridine of the transient outward current in rat ventricular cardiomyocytes. | lld:pubmed |
pubmed-article:9676733 | pubmed:affiliation | Pharmakologisches Institut der Universität Mainz, Germany. | lld:pubmed |
pubmed-article:9676733 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9676733 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:9676733 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |