Open AccessAngiotensin II accelerates mammary gland development independently of high blood pressure in pregnancy‐associated hypertensive mice
Author(s) -
Murata Kazuya,
Baasanjav Altansarnai,
Kwon Chulwon,
Hashimoto Misuzu,
Ishida Junji,
Fukamizu Akiyoshi
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12542
Subject(s) - endocrinology , medicine , mammary gland , angiotensin ii , angiotensin ii receptor type 1 , angiotensin receptor , adrenal gland , renin–angiotensin system , receptor , biology , blood pressure , breast cancer , cancer
Angiotensin II (Ang II ) is a vasopressor hormone that has critical roles in maintenance of normal blood pressure and pathogenesis of cardiovascular diseases. We previously generated pregnancy‐associated hypertensive ( PAH ) mice by mating female human angiotensinogen transgenic mice with male human renin transgenic mice. PAH mice exhibit hypertension in late pregnancy by overproducing Ang II . A recent study demonstrated that angiotensin II type I ( AT 1) receptor is expressed in mammary epithelial cells and its signaling is critical for mammary gland involution after weaning. However, the role of Ang II ‐ AT 1 receptor signaling in the development of mammary gland during pregnancy remains unclear. In this study, to investigate the role of Ang II ‐ AT 1 receptor signaling in mammary gland development during pregnancy, we analyzed the mammary gland of PAH mice. Histological and gene expression analyses revealed that lobuloalveolar development was accelerated with increased milk protein production and lipid accumulation in the mammary gland of PAH mice. Furthermore, AT 1 receptor blocker treatment suppressed acceleration of mammary gland development in PAH mice, while the treatment of hydralazine, another antihypertensive drug, did not. These data suggest that Ang II ‐ AT 1 receptor‐induced signaling accelerates mammary gland development during pregnancy through hypertension‐independent mechanism.