| pubmed-article:2316703 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2316703 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:2316703 | lifeskim:mentions | umls-concept:C1522318 | lld:lifeskim |
| pubmed-article:2316703 | lifeskim:mentions | umls-concept:C0023768 | lld:lifeskim |
| pubmed-article:2316703 | lifeskim:mentions | umls-concept:C0949653 | lld:lifeskim |
| pubmed-article:2316703 | lifeskim:mentions | umls-concept:C1367482 | lld:lifeskim |
| pubmed-article:2316703 | pubmed:issue | 3 Pt 2 | lld:pubmed |
| pubmed-article:2316703 | pubmed:dateCreated | 1990-4-23 | lld:pubmed |
| pubmed-article:2316703 | pubmed:abstractText | Angiotensin II (ANG II) is a powerful vasoconstrictor of coronary vessels and other smooth muscles. One of the actions of ANG II is the inhibition of K+ currents, possibly contributing to depolarization and contraction. Therefore, we investigated the role of ANG II on the regulation of K+ channels at the single-channel level. We studied its effect on calcium-activated potassium (KCa) channels (congruent to 250 pS) from coronary smooth muscle incorporated into lipid bilayers. KCa channels were sensitive to externally applied ANG II at voltages from -20 to -70 mV and pCa between 6.5 and 4. The dose-response curve gave a concentration of half-inhibition (Ki1/2) of 58 nM and a Hill coefficient of 2.2, indicating a minimum of two sites in the process. ANG II modified the open and closed states of the channel, affecting their proportions and their values. In addition, a new much slower (congruent to 1 s) closed or "blocked" state appeared. We conclude that one of the mechanisms by which ANG II causes vasoconstriction of the coronary vessels is a direct inhibition of KCa channels contributing to depolarization and contraction. | lld:pubmed |
| pubmed-article:2316703 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2316703 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2316703 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2316703 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2316703 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:2316703 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:2316703 | pubmed:author | pubmed-author:StefaniEE | lld:pubmed |
| pubmed-article:2316703 | pubmed:author | pubmed-author:AmadorMM | lld:pubmed |
| pubmed-article:2316703 | pubmed:author | pubmed-author:ToroLL | lld:pubmed |
| pubmed-article:2316703 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2316703 | pubmed:volume | 258 | lld:pubmed |
| pubmed-article:2316703 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2316703 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2316703 | pubmed:pagination | H912-5 | lld:pubmed |
| pubmed-article:2316703 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
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| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
| pubmed-article:2316703 | pubmed:meshHeading | pubmed-meshheading:2316703-... | lld:pubmed |
| pubmed-article:2316703 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2316703 | pubmed:articleTitle | ANG II inhibits calcium-activated potassium channels from coronary smooth muscle in lipid bilayers. | lld:pubmed |
| pubmed-article:2316703 | pubmed:affiliation | Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030. | lld:pubmed |
| pubmed-article:2316703 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2316703 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2316703 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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