Document Detail


Short-term suppression of the renin-angiotensin system in mice associated with hypertension during pregnancy.
MedLine Citation:
PMID:  22552605     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pregnancy-induced hypertension or pre-eclampsia is a major disorder that may result in serious complications for the mother and fetus. It is characterized from maternal hypertension in late pregnancy and peripheral tissue damage, including kidney, heart and placenta, and the fetus suffers from intrauterine growth retardation (IUGR) and high perinatal mortality. Recently, it has been postulated that angiotensin II (Ang II), a potent vasoconstrictor in the renin-angiotensin system (RAS), plays a pivotal role in the pathogenesis of pre-eclampsia; however, the beneficial effect of the suppression of RAS has not yet been fully elucidated. Previously, we generated a transgenic mouse model that developed pregnancy-associated hypertension (PAH) by the overproduction of Ang II in maternal circulation during late pregnancy. In addition, mice with PAH exhibited maternal and fetal abnormalities, such as proteinuria, cardiac hypertrophy, placental morphological changes and IUGR. In this study, in order to attenuate the activity of redundant RAS during the advanced stages of PAH, we administered olmesartan (Olm), an angiotensin receptor blocker, and captopril (Cp), an angiotensin converting enzyme inhibitor, from E17 to E19 days of gestation, and evaluated its effect on cardiac and placental abnormalities and fetal growth. Olm and Cp administration significantly lowered the blood pressure of mice with PAH, and placental histological change and severe IUGR were markedly ameliorated in both groups. On the contrary, Olm or Cp treatment had little effect on cardiac remodeling during the advanced stages of PAH. These findings highlight a variety of therapeutic actions of RAS repression on the progressive pathology of PAH in mice.
Authors:
Tomohiro Ishimaru; Junji Ishida; Shoko Nakamura; Misuzu Hashimoto; Tanomu Matsukura; Ayumi Nakamura; Satoshi Kunita; Fumihiro Sugiyama; Ken-Ichi Yagami; Akiyoshi Fukamizu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-04-23
Journal Detail:
Title:  Molecular medicine reports     Volume:  6     ISSN:  1791-3004     ISO Abbreviation:  Mol Med Rep     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-05-09     Completed Date:  2012-09-10     Revised Date:  2013-08-15    
Medline Journal Info:
Nlm Unique ID:  101475259     Medline TA:  Mol Med Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  28-32     Citation Subset:  IM    
Affiliation:
Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II Type 1 Receptor Blockers / administration & dosage,  pharmacology
Angiotensin-Converting Enzyme Inhibitors / administration & dosage,  pharmacology
Animals
Blood Pressure / drug effects
Captopril / administration & dosage,  pharmacology
Female
Fetal Growth Retardation / drug therapy
Hypertension, Pregnancy-Induced / etiology*
Imidazoles / administration & dosage,  pharmacology
Male
Mice
Mice, Inbred C57BL
Placenta / drug effects,  pathology
Pregnancy
Renin-Angiotensin System / drug effects*
Tetrazoles / administration & dosage,  pharmacology
Time Factors
Ventricular Remodeling / drug effects
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Imidazoles; 0/Tetrazoles; 62571-86-2/Captopril; 6M97XTV3HD/olmesartan medoxomil

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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