| pubmed-article:21708234 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0086045 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0042396 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0279023 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0917624 | lld:lifeskim |
| pubmed-article:21708234 | lifeskim:mentions | umls-concept:C0916871 | lld:lifeskim |
| pubmed-article:21708234 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:21708234 | pubmed:dateCreated | 2011-8-2 | lld:pubmed |
| pubmed-article:21708234 | pubmed:abstractText | A close link between arsenic exposure and hypertension has been well-established through many epidemiological reports, yet the mechanism underlying it remains unclear. Here we report that nanomolar concentrations of monomethylarsonous acid (MMA(III)), a toxic trivalent methylated arsenic metabolite, can potentiate agonist-induced vasoconstriction and pressor responses. In freshly isolated rat aortic ring, exposure to nanomolar MMA(III) (100-500 nM) potentiated phenylephrine (PE)-induced vasoconstriction while at higher concentrations (?2.5 ?M), suppression of vasoconstriction and apoptosis of vascular smooth muscle were observed. Potentiation of agonist-induced vasoconstriction was also observed with other contractile agonists and it was retained in endothelium-denuded aortic rings, suggesting that these events are agonist-independent and smooth muscle cell dependent. Interestingly, exposure to MMA(III) resulted in increased myosin light chain phosphorylation while PE-induced Ca2+ influx was not affected, reflecting that Ca2+ sensitization is involved. In line with this, MMA(III) enhanced agonist-induced activation of small GTPase RhoA, a key contributor to Ca2+ sensitization. Of note, treatment of MMA(III) to rats induced significantly higher pressor responses in vivo, demonstrating that this event can occur in vivo indeed. We believe that RhoA-mediated Ca2+ sensitization and the resultant potentiation of vasoconstriction by MMA(III) may shed light on arsenic-associated hypertension. | lld:pubmed |
| pubmed-article:21708234 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21708234 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21708234 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21708234 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:21708234 | pubmed:issn | 1879-3169 | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:YunYeo-PyoYP | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:ChungSeung-Mi... | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:ChungJin-HoJH | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:ShinYoo-SunYS | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:LimKyung-MinK... | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:KimKeunyoungK | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:NohJi-YoonJY | lld:pubmed |
| pubmed-article:21708234 | pubmed:author | pubmed-author:KangSeojinS | lld:pubmed |
| pubmed-article:21708234 | pubmed:copyrightInfo | Copyright © 2011. Published by Elsevier Ireland Ltd. | lld:pubmed |
| pubmed-article:21708234 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21708234 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:21708234 | pubmed:volume | 205 | lld:pubmed |
| pubmed-article:21708234 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21708234 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21708234 | pubmed:pagination | 250-6 | lld:pubmed |
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| pubmed-article:21708234 | pubmed:meshHeading | pubmed-meshheading:21708234... | lld:pubmed |
| pubmed-article:21708234 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21708234 | pubmed:articleTitle | Potentiation of vasoconstriction and pressor response by low concentration of monomethylarsonous acid (MMA(III)). | lld:pubmed |
| pubmed-article:21708234 | pubmed:affiliation | Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Republic of Korea. | lld:pubmed |
| pubmed-article:21708234 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21708234 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:21708234 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
