title: Influence of angiotensin II type 1 receptor-associated protein on prenatal development and adult hypertension after maternal dietary protein restriction during pregnancy.
abstract: An adverse relationship between suboptimal fetal environments and the development of adult diseases, such as hypertension, type II diabetes, and cardiovascular disease, has been reported in numerous studies. The purpose of this study was to investigate the strain difference of offspring's response to maternal malnutrition during pregnancy and the involvement of the renin-angiotensin system (RAS) in the development of adult hypertension using C57BL/6J (C57) mice and angiotensin II (Ang II) type 1 receptor-associated protein-transgenic (ATRAP-Tg) mice. Pregnant dams were fed an isocaloric diet containing either 20% (normal protein; NP) or 8% (low protein; LP) protein. Birth weight was significantly reduced in C57-LP offspring, but not in ATRAP-Tg-LP offspring. Arterial blood pressure was higher in C57-LP offspring than in the other groups. In contrast, ATRAP-Tg-LP offspring did not show an increase in blood pressure compared with NP offspring. Renal angiotensin II type 1 (AT(1)) receptor expression was not altered by maternal malnutrition, whereas angiotensin II type 2 receptor expression was significantly decreased in C57-LP offspring. In conclusion, these findings suggest that a suboptimal intrauterine environment induces adult hypertension because of an alteration of expression of RAS components, which was partly suppressed by sustained ATRAP overexpression via attenuation of the AT(1) receptor-mediated pathological response.
authors.affiliation: Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Tohon, Japan.
authors.forename: Kana
authors.initials: K
authors.lastname: Tsukuda
authors.forename: Masaki
authors.initials: M
authors.lastname: Mogi
authors.forename: Jun
authors.initials: J
authors.lastname: Iwanami
authors.forename: Li-Juan
authors.initials: LJ
authors.lastname: Min
authors.forename: Fei
authors.initials: F
authors.lastname: Jing
authors.forename: Kousei
authors.initials: K
authors.lastname: Ohshima
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Horiuchi
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000502:physiology; D001724:Birth Weight; D018753:Diet, Protein-Restricted / Q000009:adverse effects* / Q000379:methods; D004044:Dietary Proteins / Q000378:metabolism; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D006973:Hypertension / Q000209:etiology / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D023421:Models, Animal; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D004044:Dietary Proteins; D044140:Receptor, Angiotensin, Type 1