Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Bédard, Sylvain; Sicotte, Benoît; St‐Louis, Jean; Brochu, Martin

doi:10.1113/jphysiol.2004.064683

Cited by 22 publications

(26 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In our laboratory, an animal model of impaired foetal growth was developed by administering a low-sodium diet to rats during the last week of gestation (Roy-Clavel et al 1999), inducing an important activation of the maternal reninangiotensin-aldosterone system (RAAS) in comparison to normal pregnant rats (Bedard et al 2005). We recently showed that AT 1 R and P450aldo mRNA expression was enhanced in intrauterine growth restriction (IUGR) foetal adrenal glands and was associated with an increase in serum aldosterone levels (Bibeau et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Bibeau¹,

Otis²,

St‐Louis³

et al. 2011

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

In low sodium-induced intrauterine growth restricted (IUGR) rat, foetal adrenal steroidogenesis as well as the adult reninangiotensin-aldosterone system (RAAS) is altered. The aim of the present study was to determine the expression of cytochrome P450 aldosterone synthase (P450aldo) and of angiotensin II receptor subtypes 1 (AT 1 R) and 2 (AT 2 R) in adult adrenal glands and whether this expression could be influenced by IUGR and by high-salt intake in a sex-specific manner. After 6 weeks of 0 . 9% NaCl supplementation, plasma renin activity, P450aldo expression and serum aldosterone levels were decreased in all groups. In males, IUGR induced an increase in AT 1 R, AT 2 R, and P450aldo levels, without changes in morphological appearance of the zona glomerulosa (ZG). By contrast, in females, IUGR had no effect on the expression of AT 1 R, but increased AT 2 R mRNA while decreasing protein expression of AT 2 R and P450aldo. In males, salt intake in IUGR rats reduced both AT 1 R mRNA and protein, while for AT 2 R, mRNA levels decreased whereas protein expression increased. In females, salt intake reduced ZG size in IUGR but had no affect on AT 1 R or AT 2 R expression in either group. These results indicate that, in response to IUGR and subsequently to salt intake, P450aldo, AT 1 R, and AT 2 R levels are differentially expressed in males and females. However, despite these adrenal changes, adult IUGR rats display adequate physiological and adrenal responses to high-salt intake, via RAAS inhibition, thus suggesting that extra-adrenal factors likely compensate for ZG alterations induced by IUGR.

show abstract

Section: Introductionmentioning

confidence: 99%

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Bibeau¹,

Otis²,

St‐Louis³

et al. 2011

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Failure of this adaptation is associated with maternal morbidity/mortality and intrauterine growth restriction (3,27). Despite the progressive PVE, there is no increase in maternal blood pressure due to a marked decrease in total peripheral vascular resistance (2,7).…”

mentioning

confidence: 99%

Increased renal α-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy

West

Zhang

Ecker

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

West C, Zhang Z, Ecker G, Masilamani SM. Increased renal ␣-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy. Am J Physiol Regul Integr Comp Physiol 299: R1326 -R1332, 2010. First published August 4, 2010 doi:10.1152/ajpregu.00082.2010.-Pregnancy-mediated sodium (Na) retention is required to provide an increase in plasma volume for the growing fetus. The mechanisms responsible for this Na retention are not clear. We first used a targeted proteomics approach and found that there were no changes in the protein abundance compared with virgin rats of the ␤ or ␥ ENaC, type 3 Na ϩ /H ϩ exchanger (NHE3), bumetanide-sensitive cotransporter (NKCC2), or NaCl cotransporter (NCC) in mid-or late pregnancy. In contrast, we observed marked increases in the abundance of the ␣-ENaC subunit. The plasma volume increased progressively during pregnancy with the greatest plasma volume being evident in late pregnancy. ENaC inhibition abolished the difference in plasma volume status between virgin and pregnant rats. To determine the in vivo activity of ENaC, we conducted in vivo studies of rats in late pregnancy (days 18 -20) and virgin rats to measure the natriuretic response to ENaC blockade (with benzamil). The in vivo activity of ENaC (UNaV postbenzamil-UNaV postvehicle) was markedly increased in late pregnancy, and this difference was abolished by pretreatment with the mineralocorticoid receptor antagonist, eplerenone. These findings demonstrate that the increased ␣-ENaC subunit of pregnancy is associated with an mineralocorticoid-dependent increase in ENaC activity. Further, we show that ENaC activity is a major contributor of plasma volume status in late pregnancy. These changes are likely to contribute to the renal sodium retention and plasma volume expansion required for an optimal pregnancy. collecting duct; plasma volume expansion; sodium retention IN HUMANS AND RATS, PREGNANCY is accompanied by marked changes in cardiovascular function, renal function, and fluid homeostasis. These adaptations permit an increase in blood volume that will supply the growing uterus and fetus without the development of maternal hypertension.A normal healthy pregnancy is associated with a cumulative plasma volume expansion (PVE) (30 -50%) and avid sodium retention (2,26,27). Failure of this adaptation is associated with maternal morbidity/mortality and intrauterine growth restriction (3, 27). Despite the progressive PVE, there is no increase in maternal blood pressure due to a marked decrease in total peripheral vascular resistance (2, 7).Renal sodium excretion determines volume homeostasis and the progressive PVE of normal pregnancy must reflect net renal sodium retention. Alexander et al.(1) performed balance studies in the pregnant rat that demonstrated cumulative sodium retention during pregnancy. The reabsorption of sodium along the renal tubule is determined by the regulation of the individual tubular cotransporters and channels (16), such that a change in the activity of any transporter or channel...

show abstract

“…In women, plasma volume (PV) expands ϳ40% and is necessary for perfusion of the growing uterus, placenta, and fetus (4). Inadequate volume expansion is associated with pregnancies compromised by fetal growth restriction (3,31). Furthermore, prevention of PVE through restriction of either sodium or water intake during late pregnancy in the rat results in growthrestricted pups (28,30).…”

mentioning

confidence: 99%

Chronic vasodilation increases renal medullary PDE5A and α-ENaC through independent renin-angiotensin-aldosterone system pathways

West

Shaw

Sasser

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

West CA, Shaw S, Sasser JM, Fekete A, Alexander T, Cunningham MW Jr, Masilamani SM, Baylis C. Chronic vasodilation increases renal medullary PDE5A and ␣-ENaC through independent renin-angiotensin-aldosterone system pathways. via diet], enalapril (ENAL; angiotensin-converting enzyme inhibitor, 62.5 mg/l via water), or vehicle (CON). Mean arterial pressure (MAP) was reduced 7.4 Ϯ 0.5% with NIF, 6.33 Ϯ 0.5% with NIF ϩ SPR, 13.3 Ϯ 0.9% with NIF ϩ LOS, and 12.0 Ϯ 0.4% with ENAL vs. baseline MAP. Compared with CON (3.6 Ϯ 0.3%), plasma volume factored for body weight was increased by NIF (5.2 Ϯ 0.4%) treatment but not by NIF ϩ SPR (4.3 Ϯ 0.3%), NIF ϩ LOS (3.6 Ϯ 0.1%), or ENAL (4.0 Ϯ 0.3%). NIF increased PDE5A protein abundance in the renal inner medulla, and SPR did not prevent this increase (188 Ϯ 16 and 204 Ϯ 22% of CON, respectively). NIF increased the ␣-subunit of the epithelial sodium channel (␣-ENaC) protein in renal outer (365 Ϯ 44%) and inner (526 Ϯ 83%) medulla, and SPR prevented these changes. There was no change in either PDE5A or ␣-ENaC abundance vs. CON in rats treated with NIF ϩ LOS or ENAL. These data indicate that the PVE and renal medullary adaptations in response to chronic vasodilation result from RAAS signaling, with increases in PDE5A mediated through AT 1 receptor and ␣-ENaC through the MR.

show abstract

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Cited by 22 publications

References 56 publications

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Increased renal α-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy

Chronic vasodilation increases renal medullary PDE5A and α-ENaC through independent renin-angiotensin-aldosterone system pathways

Contact Info

Product

Resources

About