| pubmed-article:1592474 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C0003842 | lld:lifeskim |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C0596901 | lld:lifeskim |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:1592474 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1592474 | pubmed:issue | 6 Pt 2 | lld:pubmed |
| pubmed-article:1592474 | pubmed:dateCreated | 1992-6-30 | lld:pubmed |
| pubmed-article:1592474 | pubmed:abstractText | Pressurization of isolated arteries may result in Ca(2+)-dependent contraction and membrane depolarization. Because the open state probability of some vascular muscle K+ channels is augmented by rises in cytosolic Ca2+ and membrane depolarization, we investigated the possibility that increases in intraluminal pressure activate K+ channels in isolated, perfused rat saphenous arteries. Stepwise increases in intraluminal pressure from 5 to 205 mm Hg resulted in increasing, active arterial contraction, measured as smaller diameters in physiological salt solution than in Ca(2+)-free solution. Addition of 10 mM tetraethylammonium to the physiological salt solution to block arterial muscle K+ channels caused progressively greater diameter reductions at pressures above 25 mm Hg. Microelectrode measurements of membrane potential showed that tetraethylammonium depolarized arterial muscle more at 105 mm Hg (16 +/- 1 mV) than at 25 mm Hg (10 +/- 1 mV). The sensitivity of K+ current to tetraethylammonium was also demonstrated in patch-clamped vascular muscle cells from the same arteries. Peak whole-cell K+ current was suppressed 47% and 79% by 1 and 10 mM tetraethylammonium, respectively. This same current was enhanced 3.6-fold by the Ca2+ ionophore A23187 (10 microM), suggesting a Ca2+ dependence. We conclude that increases in intraluminal pressure progressively activate tetraethylammonium-sensitive K+ channels in the arterial muscle membrane. This can serve as a negative feedback mechanism to limit pressure-induced arterial constriction. | lld:pubmed |
| pubmed-article:1592474 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1592474 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1592474 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1592474 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1592474 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1592474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1592474 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1592474 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:1592474 | pubmed:issn | 0194-911X | lld:pubmed |
| pubmed-article:1592474 | pubmed:author | pubmed-author:RuschN JNJ | lld:pubmed |
| pubmed-article:1592474 | pubmed:author | pubmed-author:StekielW JWJ | lld:pubmed |
| pubmed-article:1592474 | pubmed:author | pubmed-author:ContneyS JSJ | lld:pubmed |
| pubmed-article:1592474 | pubmed:author | pubmed-author:BercziVV | lld:pubmed |
| pubmed-article:1592474 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1592474 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:1592474 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1592474 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1592474 | pubmed:pagination | 725-9 | lld:pubmed |
| pubmed-article:1592474 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:1592474 | pubmed:meshHeading | pubmed-meshheading:1592474-... | lld:pubmed |
| pubmed-article:1592474 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1592474 | pubmed:articleTitle | Pressure-induced activation of membrane K+ current in rat saphenous artery. | lld:pubmed |
| pubmed-article:1592474 | pubmed:affiliation | Department of Physiology, Medical College of Wisconsin, Milwaukee 53226. | lld:pubmed |
| pubmed-article:1592474 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1592474 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1592474 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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