Fetal functional capabilities in response to maternal hypertonicity associated with altered central and peripheral angiotensinogen mRNA in rats

Mao, Caiping; Lv, Jian; Zhu, Hong; Zhou, Yun; Chen, Rongzheng; Feng, Xin; Cui, Yugui; Wang, Chen; Hui, Pengpeng; Xu, Fulin; Xu, Zhice

doi:10.1016/j.peptides.2007.03.018

Cited by 11 publications

(9 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of factors during pregnancy, including dehydration, high salt intake, and drugs, may cause changes in fetal body fluids (Mao et al, 2007). In the present study, tanshinone IIA infusion into the maternal animal, no matter high or low the doses, did not initiate any significant change in fetal body-fluid regulatory and renal systems, as evidenced by the fact that volume and osmolality in fetal urine remained the same following tanshinone IIA applications.…”

Section: Discussionsupporting

confidence: 40%

The effect of tanshinone IIA on renal and liver functions in ovine fetusesin utero

Zhang¹,

Rui²,

Mao³

et al. 2009

Drug and Chemical Toxicology

Self Cite

View full text Add to dashboard Cite

This was the first study in determination of the effects of the herbal medicine, danshen, on fetal hepatic and renal functions in utero. Tanshinone IIA, an active ingredient of danshen, was tested in the experimental fetal model. Three doses (20, 40, or 80 mg) of tanshinone IIA and 0.9% NaCl (as the control) were intravenously (i.v.) administrated into pregnant ewes. Both maternal and fetal blood samples were collected and analyzed for renal and liver functions by examining the enzymes and renal excretion. The results showed that tanshinone IIA did not alter fetal urine volume, urine electrolytes, and osmolality. Enzyme activities related to the hepatic and renal functions were not changed. In addition, maternal application of tanshinone IIA had no effect of maternal and fetal lipid profile. The results demonstrated that tanshinone IIA used during the last third of gestation did not cause the biochemical changes related to renal and liver functions in both the mother and fetus. This provides new information to guide the use of herbal medicine during pregnancy.

show abstract

Section: Discussionsupporting

confidence: 40%

The effect of tanshinone IIA on renal and liver functions in ovine fetusesin utero

Zhang¹,

Rui²,

Mao³

et al. 2009

Drug and Chemical Toxicology

Self Cite

View full text Add to dashboard Cite

show abstract

“…hrs) [37]. However, after maternal administration of a NaCl bolus, recovery of fetal plasma osmolality back to baseline had occured by 9 h in the fetal but not maternal circulation, indicating an independent role for the placenta in modifying the fetal environment [37]. Indeed, our data would suggest just such an effect after long-term (days-weeks) elevated sodium exposure, given no difference in fetal electrolyte concentrations.…”

Section: Discussionmentioning

confidence: 60%

“…Previous studies have shown in the late gestation rat fetus that the fetal circulation may mirror plasma sodium fluctuations in the maternal circulation in the short-term (i.e. hrs) [37]. However, after maternal administration of a NaCl bolus, recovery of fetal plasma osmolality back to baseline had occured by 9 h in the fetal but not maternal circulation, indicating an independent role for the placenta in modifying the fetal environment [37].…”

Section: Discussionmentioning

confidence: 93%

Excess Maternal Salt Intake Produces Sex-Specific Hypertension in Offspring: Putative Roles for Kidney and Gastrointestinal Sodium Handling

et al. 2013

View full text Add to dashboard Cite

Hypertension is common and contributes, via cardiovascular disease, towards a large proportion of adult deaths in the Western World. High salt intake leads to high blood pressure, even when occurring prior to birth – a mechanism purported to reside in altered kidney development and later function. Using a combination of in vitro and in vivo approaches we tested whether increased maternal salt intake influences fetal kidney development to render the adult individual more susceptible to salt retention and hypertension. We found that salt-loaded pregnant rat dams were hypernatraemic at day 20 gestation (147±5 vs. 128±5 mmoles/L). Increased extracellular salt impeded murine kidney development in vitro, but had little effect in vivo. Kidneys of the adult offspring had few structural or functional abnormalities, but male and female offspring were hypernatraemic (166±4 vs. 149±2 mmoles/L), with a marked increase in plasma corticosterone (e.g. male offspring; 11.9 [9.3–14.8] vs. 2.8 [2.0–8.3] nmol/L median [IQR]). Furthermore, adult male, but not female, offspring had higher mean arterial blood pressure (effect size, +16 [9–21] mm Hg; mean [95% C.I.]. With no clear indication that the kidneys of salt-exposed offspring retained more sodium per se, we conducted a preliminary investigation of their gastrointestinal electrolyte handling and found increased expression of proximal colon solute carrier family 9 (sodium/hydrogen exchanger), member 3 (SLC9A3) together with altered faecal characteristics and electrolyte handling, relative to control offspring. On the basis of these data we suggest that excess salt exposure, via maternal diet, at a vulnerable period of brain and gut development in the rat neonate lays the foundation for sustained increases in blood pressure later in life. Hence, our evidence further supports the argument that excess dietary salt should be avoided per se, particularly in the range of foods consumed by physiologically immature young.

show abstract

“…Several important nuclei located around the ventricular area, including the paraventricular nuclei, subfornical organ, median preoptic nuclei, and supraoptic nuclei, play an important role in water and salt intake in response to i.c.v. Ang II (Fitzsimons, 1998; Davisson et al, 2000; Mao et al, 2007a, b). Those areas around the ventricular system are also rich of Ang II receptors (Fitzsimons, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Maternal, fetal, and adult offspring blood samples were collected into ice-cold plastic tubes as reported (Mao et al, 2007a, b). Briefly, fetal blood samples (7–8 fetuses from the same dam as n =1, and n =6–8, each group) were collected directly from the heart using intracardiac puncture, and blood was pooled together in the same litter.…”

Section: Methodsmentioning

confidence: 99%

Prenatal water deprivation alters brain angiotensin system and dipsogenic changes in the offspring

et al. 2011

Self Cite

View full text Add to dashboard Cite

Objective 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. Methods Pregnant rats were deprived of water during late gestation. Expressions of brain angiotensinogen, angiotensin II receptors, and dipsogenic responses were determined. Results Maternal water deprivation significantly decreased fetal body and brain weight, and body and tail length. Fetal plasma sodium, osmolality, and hematocrit were increased. Both AT1R and AT2R protein abundance was significantly increased in the fetal brain, associating with increased mRNA levels of AT1aR and AT2R. Additionally, angiotensinogen mRNA was increased. In adult offspring, prenatal dehydration resulted in significant increases in AT1R protein and AT1aR mRNA, as well as angiotensinogen mRNA in the forebrain in both males and females. In contrast, AT2R 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. Conclusion 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.

show abstract

Fetal functional capabilities in response to maternal hypertonicity associated with altered central and peripheral angiotensinogen mRNA in rats

Cited by 11 publications

References 35 publications

The effect of tanshinone IIA on renal and liver functions in ovine fetusesin utero

The effect of tanshinone IIA on renal and liver functions in ovine fetusesin utero

Excess Maternal Salt Intake Produces Sex-Specific Hypertension in Offspring: Putative Roles for Kidney and Gastrointestinal Sodium Handling

Prenatal water deprivation alters brain angiotensin system and dipsogenic changes in the offspring

Contact Info

Product

Resources

About