Prenatal dehydration alters renin-angiotensin system associated with angiotensin-increased blood pressure in young offspring.
The renin-angiotensin system (RAS) has an important role in cardiovascular homeostasis. This study determined the influence of water deprivation during pregnancy on the development of the RAS in rats, and examined blood pressure (BP) in the adolescent offspring. Pregnant rats were water deprived for 3 days at late gestation, and we examined fetal cardiac ultrastructure, as well as heart angiotensin (Ang) II receptor protein and mRNA, liver angiotensinogen and plasma Ang II concentrations. We also tested cardiovascular responses to i.v. Ang II in the young offspring. In utero exposure to maternal water deprivation significantly decreased fetal body and heart weight, and increased fetal plasma sodium and osmolality. Fetal liver angiotensinogen mRNA, plasma Ang I and Ang II concentrations were also increased. Although fetal AT(1a) and AT(1b) receptor mRNA and AT(1) protein were not changed, AT(2) receptor mRNA and protein levels in the heart were significantly increased following maternal dehydration. Prenatal exposure to maternal water deprivation had no effect on baseline BP; however, it significantly increased BP in response to i.v. Ang II infusion, and decreased baroreflex sensitivity in the offspring. In addition, the heart AT(2) receptor mRNA and protein were higher in the offspring exposed to prenatal dehydration. The results of this study demonstrate that prenatal dehydration affected the RAS development associated with an Ang II-increased BP in fetal origin.
Perinatal Biology Center, Soochow University First Affiliated Hospital, Suzhou, China.
Junchang
J
Guan
Caiping
C
Mao
Feichao
F
Xu
Chunsong
C
Geng
Liyan
L
Zhu
Aiqing
A
Wang
Zhice
Z
Xu
D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000808:Angiotensinogen / Q000235:genetics; D000818:Animals; D017704:Baroreflex / Q000502:physiology; D001724:Birth Weight; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D047109:Fetal Development; D015870:Gene Expression / Q000502:physiology; D006321:Heart / Q000196:embryology / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology*; D008099:Liver / Q000196:embryology / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D014868:Water Deprivation / Q000502:physiology*
D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D000808:Angiotensinogen; D000804:Angiotensin II; D000803:Angiotensin I