Abstract
BackgroundHypertension may result from high-fat (HF) diet induced-obesity and overexposure to glucocorticoids in utero. Recent studies demonstrated the potent contribution of adipose tissue’s renin-angiotensin system (RAS) to systemic RAS, which plays a key role in regulating blood pressure (BP). In this study, we investigated the effects of prenatal dexamethasone (DEX) exposure and postnatal HF diet on RAS of adipose tissue.MethodsRAS and BP of 6-month old rats exposed to prenatal DEX and/or postnatal HF diet were examined.ResultsPrenatal DEX plus postnatal HF exerted a synergistic effect on systolic BP. Prenatal DEX exposure suppressed plasma angiotensin (ANG) I and ANG II, whereas postnatal HF suppressed plasma ANG-(1–7) level. Prenatal DEX increased prorenin receptor and renin levels, but suppressed angiotensinogen (AGT) and angiotensin-converting-enzyme 1 (ACE1) mRNA expressions in adipose tissue. Postnatal HF increased AGT mRNA expression, but suppressed prorenin receptor, renin, ACE2, ANG II type 2 receptor (AT2R), and Mas receptor (MasR) mRNA expression levels.ConclusionsPrenatal GC exposure altered the ACE1/ANG II/ANG II type 1 receptor (AT1R) axis, whereas postnatal HF negatively impacted the ACE2/ANG-(1–7)/MasR axis. Prenatal DEX exposure and postnatal HF synergistically elevated BP through a distinct programming mechanism of systemic and adipose RAS. Adipose RAS might be a target for precise hypertension treatment.
Highlights
Hypertension may result from high-fat (HF) diet induced-obesity and overexposure to glucocorticoids in utero
All statistical analyses were performed using SPSS 19.0 for Windows XP (SPSS, Inc., Chicago, IL, USA). Both prenatal DEX exposure and postnatal HF diet increased body weight and blood pressure (BP) in offspring at 6 M In our study, we found there is no difference in the litter size and ratio of male-to-female pups as reported earlier [16]
We found that the expression of Angiotensin-converting-enzyme 2 (ACE2) mRNA in retroperitoneal adipose tissue decreased with long-term HF diet in rats
Summary
Hypertension may result from high-fat (HF) diet induced-obesity and overexposure to glucocorticoids in utero. We investigated the effects of prenatal dexamethasone (DEX) exposure and postnatal HF diet on RAS of adipose tissue. If preterm delivery is expected, glucocorticoid (GC) treatment is given to stimulate the development of the fetal lungs and decrease the postnatal mortality and morbidity [7,8,9]. Our previous studies support these adverse effects of prenatal GC over-exposure during fetal development [12, 14,15,16,17]. We showed that dexamethasone (DEX) treatment during pregnancy enhances the susceptibility of the offspring to postnatal HF diet-induced programmed hypertension [18]. The causes for the induction of hypertension by prenatal DEX may include a decrease in the number of nephrons and altered levels of luminal ANG II and sodium transporter [13, 19, 20]
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