| pubmed-article:12372799 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12372799 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:12372799 | lifeskim:mentions | umls-concept:C0221464 | lld:lifeskim |
| pubmed-article:12372799 | lifeskim:mentions | umls-concept:C0027103 | lld:lifeskim |
| pubmed-article:12372799 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12372799 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:12372799 | pubmed:dateCreated | 2002-10-9 | lld:pubmed |
| pubmed-article:12372799 | pubmed:abstractText | The initiation of contractile force in arterial smooth muscle (SM) is believed to be regulated by the intracellular Ca2+ concentration and SM myosin type II phosphorylation. We tested the hypothesis that SM myosin type II operates as a molecular motor protein in electromechanical, but not in protein kinase C (PKC)-induced, contraction of small resistance-sized cerebral arteries. We utilized a SM type II myosin heavy chain (MHC) knockout mouse model and measured arterial wall Ca2+ concentration ([Ca2+](i)) and the diameter of pressurized cerebral arteries (30-100 microm) by means of digital fluorescence video imaging. Intravasal pressure elevation caused a graded [Ca2+](i) increase and constricted cerebral arteries of neonatal wild-type mice by 20-30%. In contrast, intravasal pressure elevation caused a graded increase of [Ca2+](i) without constriction in (-/-) MHC-deficient arteries. KCl (60 mM) induced a further [Ca2+](i) increase but failed to induce vasoconstriction of (-/-) MHC-deficient cerebral arteries. Activation of PKC by phorbol ester (phorbol 12-myristate 13-acetate, 100 nM) induced a strong, sustained constriction of (-/-) MHC-deficient cerebral arteries without changing [Ca2+](i). These results demonstrate a major role for SM type II myosin in the development of myogenic tone and Ca2+ -dependent constriction of resistance-sized cerebral arteries. In contrast, the sustained contractile response did not depend on myosin and intracellular Ca2+ but instead depended on PKC. We suggest that SM myosin type II operates as a molecular motor protein in the development of myogenic tone but not in pharmacomechanical coupling by PKC in cerebral arteries. Thus PKC-dependent phosphorylation of cytoskeletal proteins may be responsible for sustained contraction in vascular SM. | lld:pubmed |
| pubmed-article:12372799 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12372799 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12372799 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12372799 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12372799 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:12372799 | pubmed:issn | 0363-6143 | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:LuftFriedrich... | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:HallerHermann... | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:GollaschMaikM | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:LöhnMatthiasM | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:KämpfDietmarD | lld:pubmed |
| pubmed-article:12372799 | pubmed:author | pubmed-author:Gui-XuanChaiC | lld:pubmed |
| pubmed-article:12372799 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12372799 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:12372799 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12372799 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12372799 | pubmed:pagination | C1383-9 | lld:pubmed |
| pubmed-article:12372799 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
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| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:meshHeading | pubmed-meshheading:12372799... | lld:pubmed |
| pubmed-article:12372799 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12372799 | pubmed:articleTitle | Regulation of arterial tone by smooth muscle myosin type II. | lld:pubmed |
| pubmed-article:12372799 | pubmed:affiliation | Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine, Charité University Hospital, Humboldt University of Berlin, 13125 Berlin, Germany. | lld:pubmed |
| pubmed-article:12372799 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12372799 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:17880 | entrezgene:pubmed | pubmed-article:12372799 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12372799 | lld:pubmed |
