| pubmed-article:16920816 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C0003483 | lld:lifeskim |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C0018338 | lld:lifeskim |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16920816 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:16920816 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16920816 | pubmed:dateCreated | 2007-1-10 | lld:pubmed |
| pubmed-article:16920816 | pubmed:abstractText | GMP affects vascular tone by multiple mechanisms, including inhibition of the Rho/Rho kinase-mediated Ca(2+) sensitization, a process identified as Ca(2+) desensitization. Ca(2+) desensitization is mediated probably by both cGMP- and cAMP-dependent protein kinases (cGKI and PKA). We investigate to which extent Ca(2+) desensitization is initiated by cGKI and PKA. cGMP/cAMP-induced relaxation was studied at constant [Ca(2+)] in permeabilized aortas from wild-type and cGKI-deficient mice. [Ca(2+)] increased aortic tone in the absence and presence of 50 microM GTPgammaS with EC(50) values of 160 and 30 nM, respectively. In the absence of GTPgammaS, the EC(50) for [Ca(2+)] was shifted rightward from 0.16 microM to 0.43 and 0.82 microM by 1 and 300 microM 8-bromo-cGMP (8-Br-cGMP), and to 8 microM by 10 microM Y-27632. Contractions induced by 300 nM [Ca(2+)] were relaxed by 8-Br-cGMP with an EC(50) of 2.6 microM. Surprisingly, [Ca(2+)]-induced contractions were also relaxed by 8-Br-cGMP in aortas from cGKI(-/-) mice (EC(50) of 19 microM). Western blot analysis of the vasodilator-stimulated phosphoprotein indicated "cross"-activation of PKA by 1 mM 8-Br-cGMP in aortic smooth muscle cells from cGKI(-/-) mice. Indeed, the PKA inhibitor peptide (PKI 5-24) completely abolished the relaxant effect of 8-Br-cGMP in muscles from cGKI(-/-) mice and to 65% in wild-type aortas. The thromboxane analogue U-46619 induced contraction at constant [Ca(2+)], which was only partially relaxed by 8-Br-cGMP but completely relaxed by Y-27632. The effect of 8-Br-cGMP on U-46619-induced contraction was attenuated by PKI 5-24. These results show that cGKI has only a small inhibitory effect on Ca(2+) sensitization in murine aortas. | lld:pubmed |
| pubmed-article:16920816 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16920816 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16920816 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16920816 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16920816 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16920816 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16920816 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16920816 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16920816 | pubmed:issn | 0363-6135 | lld:pubmed |
| pubmed-article:16920816 | pubmed:author | pubmed-author:HofmannFranzF | lld:pubmed |
| pubmed-article:16920816 | pubmed:author | pubmed-author:WegenerJörg... | lld:pubmed |
| pubmed-article:16920816 | pubmed:author | pubmed-author:WörnerRenéR | lld:pubmed |
| pubmed-article:16920816 | pubmed:author | pubmed-author:LukowskiRober... | lld:pubmed |
| pubmed-article:16920816 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16920816 | pubmed:volume | 292 | lld:pubmed |
| pubmed-article:16920816 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16920816 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16920816 | pubmed:pagination | H237-44 | lld:pubmed |
| pubmed-article:16920816 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:meshHeading | pubmed-meshheading:16920816... | lld:pubmed |
| pubmed-article:16920816 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:16920816 | pubmed:articleTitle | cGMP signals mainly through cAMP kinase in permeabilized murine aorta. | lld:pubmed |
| pubmed-article:16920816 | pubmed:affiliation | Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Str. 29, 80802 München, Germany. | lld:pubmed |
| pubmed-article:16920816 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16920816 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:19091 | entrezgene:pubmed | pubmed-article:16920816 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16920816 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16920816 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16920816 | lld:pubmed |
