ABSTRACT: Central renin-angiotensin system (RAS) plays an important role in regulating body fluid balance. The present study determined the effect of maternal dehydration on brain expression levels of angiotensinogen, angiotensin II receptor subtypes, and dipsogenic responses in offspring.
Pregnant rats were deprived of water during late gestation. Expressions of brain angiotensinogen, angiotensin II receptors, and dipsogenic responses were determined.
Maternal water deprivation significantly decreased fetal body and brain weight, and body and tail length. Fetal plasma sodium, osmolality, and hematocrit were increased. Both AT(1)R and AT(2)R protein abundance was significantly increased in the fetal brain, associating with increased mRNA levels of AT(1a)R and AT(2)R. Additionally, angiotensinogen mRNA was increased. In adult offspring, prenatal dehydration resulted in significant increases in AT(1)R protein and AT(1a)R mRNA, as well as angiotensinogen mRNA in the forebrain in both males and females. In contrast, AT(2)R mRNA and protein were increased only in males. Prenatal dehydration resulted in a significant increase in intracerebroventricular angiotensin II-induced water intake in male, but not female, offspring.
The results provided new information that antenatal water deprivation induces a reprogramming of brain RAS and Ang II receptor expression patterns and alters the central Ang II-mediated dipsogenic response in offspring in a sex-dependent manner.
Brain research 01/2011; 1382:128-36. · 2.46 Impact Factor
ABSTRACT: Cholinergic regulation is important in the control of cardiovascular and endocrine responses. The mechanisms behind cardiovascular responses induced by cholinergic activation are explored by studying hormonal systems, including renin-angiotensin and vasopressin (VP).
In chronically prepared fetal sheep, intravenous infusion of the cholinergic agonist carbachol increased fetal systolic, diastolic, and mean arterial pressure accompanied with bradycardia at near-term. Although intravenous administration of carbachol had no effect on plasma VP concentrations, this agonist increased angiotensin I and angiotensin II levels in fetal plasma. Fetal blood values, including sodium, osmolality, nitric oxide, hemoglobin, and hematocrit were unchanged by intravenous carbachol.
Cholinergic activation by carbachol controls fetal blood pressure and heart rate in utero. An over-activated fetal renin-angiotensin-system (RAS) is associated with changes in vascular pressure following intravenous administration of carbachol, indicating that the cholinergic stimulation-mediated hormonal mechanism in the fetus might play a critical role in the regulation of cardiovascular homeostasis.
Journal of Perinatal Medicine 11/2009; 38(1):71-6. · 1.70 Impact Factor
ABSTRACT: 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.
Hypertension Research 09/2009; 32(12):1104-11. · 2.58 Impact Factor