Central angiotensin I increases fetal AVP neuron activity and pressor responses

Shi, Lijun; Mao, Caiping; Zeng, Fanxing; Hou, Jianquan; Zhang, Hong; Xu, Zhice

doi:10.1152/ajpendo.00060.2010

Cited by 11 publications

(4 citation statements)

References 34 publications

(43 reference statements)

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“…However, functional experiments do not support this postulation. As we indicated above, in the ovine fetus both central and peripheral administration of Ang II elicited a significant increase in blood pressure26, 60 which was completely abolished by the AT1R blocker losartan, but not by the AT2R blocker PD123319. 21,25 These findings directly contradict the data derived from binding assays that the AT2R is the predominant Ang II receptor subtype in fetal life.…”

Section: Discussionmentioning

confidence: 79%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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In the current experiment, we determined AT2R and AT1R protein expression by Western blot analysis in developing normal mice. The results indicate that, (1) in all detected brain regions and in the spinal cord, adult mice exhibited significantly higher AT2R expression and lower AT1R expression in total protein extracts compared to fetuses and neonates; (2) other major organs, including heart, lung, liver, and kidney, exhibited the same expression pattern as the brain and spinal cord; (3) reciprocal changes in AT2R and AT1R expression were found in the total protein extracts from the brainstems of mice from one day prenatal to six weeks of age. There was a negative correlation between AT2R and AT1R protein expression; (4) in both membrane and cytosolic fractions from the brainstem, adult mice exhibited higher AT2R and lower AT1R expression than did fetuses and neonates; (5) in the brainstem, there were no significant differences in AT2R and AT1R mRNA levels among fetal, neonatal, and adult mice. The above results reconfirmed our previous finding in rats that adult animals have higher AT2R and lower AT1R expression compared to fetuses and neonates. These data imply an involvement of AT1R in fetal development and of AT2R in adult function.

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Section: Discussionmentioning

confidence: 79%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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show abstract

“…Mediated by a wide range of neurotransmitters and hormones, another possible explanation for our observations can be that pressure directed to the fetal head causes a vagal reflex with ensuing bradycardia and vasodilation causing, in turn, an increase in PI and PSV. The Renin-Angiotensin system is another possible mediator of such changes in the fetal brain [9].…”

Section: Discussionmentioning

confidence: 99%

The Effect of the Pressure Exerted on the Maternal Abdominal Wall by the US Probe on Fetal MCA Peak Systolic Velocity

et al. 2015

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To quantify the pressure exerted on the maternal abdominal wall during ultrasound examination and evaluate its effect on the fetal middle cerebral artery (MCA) peak systolic velocity (PSV). Gravid women with singleton pregnancies in their 2nd-3 rd trimester undergoing fetal sonographic evaluation for various indications were recruited. Each subject underwent transabdominal US measuring fetal distance from the probe, abdominal thickness, amniotic fluid index and biophysical profile. The applied pressure was measured simultaneously using an electronic pressure sensor attached directly to the US probe. For each subject baseline values of the pressure required for proper visualization were obtained. Fetal MCA was then demonstrated using color Doppler US. The PSV was measured at different pressure ranges with each subject used as her own control. Care was taken not to exceed the baseline pressure for each subject. 29 women were recruited. 24 subjects (82.7 %) demonstrated a statistically significant positive correlation between the pressure exerted and MCA-PSV (R-0.37, p < 0.0001). Of these, 4 subjects (13.8 % of study population) demonstrated elevation of PSV values above 1.29 MOM and 5 subjects (17.2 %) demonstrated elevation of PSV values above 1.5 MOM for gestational age with increasing pressure. In total, 9 subjects (31 %) demonstrated significant changes in the MCA-PSV measurements (owing to increase in pressure applied) that could potentially falsely influence clinical obstetric diagnosis and management. The pressure exerted on the maternal abdominal wall during US examination is an important parameter, producing clinically significant measurable changes in fetal MCA hemodynamics. Further study is needed in order to demonstrate the potential effect of pressure as a parameter influencing the diagnostic accuracy of the MCA-PSV in the setting of fetal anemia.

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“…Previously, arterial BP was found to correlate with pulmonary ACE concentration in sheep fetuses infused with either dexamethasone or saline ( 23 ). Pulmonary ACE is responsible both for the production of vasoconstrictive AII and for the degradation of the vasodilator bradykinin, and the RAS is known to have an important role in the control of fetal BP by peripheral and central mechanisms ( 55 – 57 ). Furthermore, the RAS has been implicated in the developmental programming of hypertension in sheep and rodent offspring exposed to glucocorticoids in utero ( 58 – 60 ).…”

Section: Discussionmentioning

confidence: 99%

Maternal Dexamethasone Treatment Alters Tissue and Circulating Components of the Renin-Angiotensin System in the Pregnant Ewe and Fetus

et al. 2015

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Antenatal synthetic glucocorticoids promote fetal maturation in pregnant women at risk of preterm delivery and their mechanism of action may involve other endocrine systems. This study investigated the effect of maternal dexamethasone treatment, at clinically relevant doses, on components of the renin-angiotensin system (RAS) in the pregnant ewe and fetus. From 125 days of gestation (term, 145 ± 2 d), 10 ewes carrying single fetuses of mixed sex (3 female, 7 male) were injected twice im, at 10–11 pm, with dexamethasone (2 × 12 mg, n = 5) or saline (n = 5) at 24-hour intervals. At 10 hours after the second injection, maternal dexamethasone treatment increased angiotensin-converting enzyme (ACE) mRNA levels in the fetal lungs, kidneys, and heart and ACE concentration in the circulation and lungs, but not kidneys, of the fetuses. Fetal cardiac mRNA abundance of angiotensin II (AII) type 2 receptor decreased after maternal dexamethasone treatment. Between the two groups of fetuses, there were no significant differences in plasma angiotensinogen or renin concentrations; in transcript levels of renal renin, or AII type 1 or 2 receptors in the lungs and kidneys; or in pulmonary, renal or cardiac protein content of the AII receptors. In the pregnant ewes, dexamethasone administration increased pulmonary ACE and plasma angiotensinogen, and decreased plasma renin, concentrations. Some of the effects of dexamethasone treatment on the maternal and fetal RAS were associated with altered insulin and thyroid hormone activity. Changes in the local and circulating RAS induced by dexamethasone exposure in utero may contribute to the maturational and tissue-specific actions of antenatal glucocorticoid treatment.

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Central angiotensin I increases fetal AVP neuron activity and pressor responses

Cited by 11 publications

References 34 publications

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

The Effect of the Pressure Exerted on the Maternal Abdominal Wall by the US Probe on Fetal MCA Peak Systolic Velocity

Maternal Dexamethasone Treatment Alters Tissue and Circulating Components of the Renin-Angiotensin System in the Pregnant Ewe and Fetus

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