| pubmed-article:19124433 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19124433 | lifeskim:mentions | umls-concept:C0032961 | lld:lifeskim |
| pubmed-article:19124433 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
| pubmed-article:19124433 | lifeskim:mentions | umls-concept:C0205373 | lld:lifeskim |
| pubmed-article:19124433 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:19124433 | pubmed:dateCreated | 2009-1-6 | lld:pubmed |
| pubmed-article:19124433 | pubmed:abstractText | Pregnancy is characterized by an increase in many of the different components of the circulating renin-angiotensin system (RAS). However, the physiological mechanisms of stimulated RAS activity during pregnancy are unknown. Even less understood is how this system may be altered in pre-eclampsia, a hypertensive disorder of pregnancy. Additional studies have shown the presence of a local tissue specific RAS in the uteroplacental unit of normal and pre-eclamptic pregnancies. Differences in normal pregnant and pre-eclamptic RAS component regulation may provide insight into the mechanisms responsible for the clinical pathological features of pre-eclampsia. Specifically, this review summarizes the key findings in the circulating and uteroplacental RAS in normal and pre-eclamptic pregnancies. | lld:pubmed |
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| pubmed-article:19124433 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19124433 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124433 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19124433 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19124433 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:19124433 | pubmed:issn | 1753-9447 | lld:pubmed |
| pubmed-article:19124433 | pubmed:author | pubmed-author:BrosnihanK... | lld:pubmed |
