| pubmed-article:14709821 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C0003483 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C1413221 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:14709821 | lifeskim:mentions | umls-concept:C1140999 | lld:lifeskim |
| pubmed-article:14709821 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:14709821 | pubmed:dateCreated | 2004-1-7 | lld:pubmed |
| pubmed-article:14709821 | pubmed:abstractText | CD38 is an ectoenzyme with ADP-ribosyl cyclase and hydrolase activities, which synthesizes cyclic ADP-ribose from NAD and hydrolyzes cyclic ADP-ribose to ADP-ribose. It has been shown that cyclic ADP-ribose is a potent Ca(2+) mobilizing messenger in many cells. To know the physiological role of cyclic ADP-ribose in vascular smooth muscle, we examined the effects of various agonists in the aorta isolated from CD38 knockout (CD38(-/-)) mouse. Western blot analysis showed that CD38 protein was detected in the aorta isolated from wild-type (CD38(+/+)) mouse, but not from CD38(-/-) mouse. In the aortae isolated from both CD38(+/+) and CD38(-/-) mice, KCl, phenylephrine and norepinephrine induced concentration-dependent contraction. KCl produced similar concentration-dependent responses in the aortae from both CD38(+/+) and CD38(-/-) mice. Maximum force of contraction induced by KCl (65 mM) was same in the size. Phenylephrine- and norepinephrine-induced contractions were, however, significantly smaller in the aortae from CD38(-/-) mice than in those from CD38(+/+) mice. 5-Hydroxytryptamine, endothelin-1, caffeine and thapsigargin-induced contractions were not significantly different in these two aortae. These results suggest that CD38 gene disruption inhibits alpha-adrenoceptor-induced vascular contractions and cyclic ADP-ribose-mediated signal transduction system is committed in these responses. | lld:pubmed |
| pubmed-article:14709821 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14709821 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14709821 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14709821 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14709821 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14709821 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:14709821 | pubmed:issn | 0916-7250 | lld:pubmed |
| pubmed-article:14709821 | pubmed:author | pubmed-author:KatoIchiroI | lld:pubmed |
| pubmed-article:14709821 | pubmed:author | pubmed-author:TakasawaShinS | lld:pubmed |
| pubmed-article:14709821 | pubmed:author | pubmed-author:OkamotoHirosh... | lld:pubmed |
| pubmed-article:14709821 | pubmed:author | pubmed-author:Mitsui-SaitoM... | lld:pubmed |
| pubmed-article:14709821 | pubmed:author | pubmed-author:YanagisawaTer... | lld:pubmed |
| pubmed-article:14709821 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14709821 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:14709821 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14709821 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14709821 | pubmed:pagination | 1325-30 | lld:pubmed |
| pubmed-article:14709821 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:14709821 | pubmed:meshHeading | pubmed-meshheading:14709821... | lld:pubmed |
| pubmed-article:14709821 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14709821 | pubmed:articleTitle | CD38 gene disruption inhibits the contraction induced by alpha-adrenoceptor stimulation in mouse aorta. | lld:pubmed |
| pubmed-article:14709821 | pubmed:affiliation | Department of Molecular Pharmacology, Graduate School of Medicine, Tohoku University, Sendai, Japan. | lld:pubmed |
| pubmed-article:14709821 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14709821 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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