Role of the renin-angiotensin system in the development of the ureteric bud and renal collecting system

Yosypiv, Ihor V.; El‐Dahr, Samir S.

doi:10.1007/s00467-005-1944-3

Cited by 31 publications

(57 citation statements)

References 86 publications

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“…This opposite effect of AT 1 and AT 2 receptors, namely a stimulatory effect of AT 1 and inhibitory effect of AT 2 , is also described on other tissues (34)(35)(36)(37)(38)(39).…”

Section: Discussionmentioning

confidence: 75%

“…ANGII and AT 2 receptor antagonist treatment induced an increase in lung branching by the stimulation of p44/42 and Akt phosphorylation. These intracellular mediators are also involved in AT 1 effects on proliferation and survival of cells in other tissues (34,36). Regarding lung growth inhibition induced by AT 1 antagonist, it was mediated by a decrease of p-38 and JNK phosphorylation.…”

Section: Discussionmentioning

confidence: 98%

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Local Fetal Lung Renin-Angiotensin System as a Target to Treat Congenital Diaphragmatic Hernia

Nogueira‐Silva

Carvalho-Dias

Piairo

et al. 2011

Mol Med

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Antenatal stimulation of lung growth is a reasonable approach to treat congenital diaphragmatic hernia (CDH), a disease characterized by pulmonary hypoplasia and hypertension. Several evidences from the literature demonstrated a possible involvement of renin-angiotensin system (RAS) during fetal lung development. Thus, the expression pattern of renin, angiotensin-converting enzyme, angiotensinogen, type 1 (AT 1 ) and type 2 (AT 2 ) receptors of angiotensin II (ANGII) was assessed by immunohistochemistry throughout gestation, whereas the function of RAS in the fetal lung was evaluated using fetal rat lung explants. These were morphometrically analyzed and intracellular pathway alterations assessed by Western blot. In nitrofen-induced CDH model, pregnant rats were treated with saline or PD-123319. In pups, lung growth, protein/DNA ratio, radial saccular count, epithelial differentiation and lung maturation, vascular morphometry, right ventricular hypertrophy and overload molecular markers, gasometry and survival time were evaluated. Results demonstrated that all RAS components were constitutively expressed in the lung during gestation and that ANGII had a stimulatory effect on lung branching, mediated by AT 1 receptor, through p44/42 and Akt phosphorylation. This stimulatory effect on lung growth was mimicked by AT 2 -antagonist (PD-123319) treatment. In vivo antenatal PD-123319 treatment increased lung growth, ameliorated indirect parameters of pulmonary hypertension, improved lung function and survival time in nonventilated CDH pups, without maternal or fetal deleterious effects. Therefore, this study demonstrated a local and physiologically active RAS during lung morphogenesis. Moreover, selective inhibition of AT 2 receptor is presented as a putative antenatal therapy for CDH.

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“…This opposite effect of AT 1 and AT 2 receptors, namely a stimulatory effect of AT 1 and inhibitory effect of AT 2 , is also described on other tissues (34)(35)(36)(37)(38)(39).…”

Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 98%

Local Fetal Lung Renin-Angiotensin System as a Target to Treat Congenital Diaphragmatic Hernia

Nogueira‐Silva

Carvalho-Dias

Piairo

et al. 2011

Mol Med

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“…Immunoreactive AT1 was decreased at 78 dG, whereas renin was increased in the RC kidneys at dG 135 but not at 78 dG. Previous authors have suggested AT1 as an important mediator of branching morphogenesis in the fetal kidney (34). Others have demonstrated dysregulation of the intrarenal RAS in rat models of programmed hypertension (8,17,35,36).…”

Section: Discussionmentioning

confidence: 92%

Nutrient Restriction Impairs Nephrogenesis in a Gender-Specific Manner in the Ovine Fetus

et al. 2007

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Inadequate nutrition compromises fetal development and poses long-term health risks for the offspring, even without decreased birth weight. The present study sought to 1) establish the ontogeny of fetal renal glomerulus number (GN) in sheep and 2) evaluate the effects of 50% global nutrient restriction (NR) during early to midgestation on GN and the renin-angiotensin system in the fetal kidney. GN increased from 78 dG (68,560 Ϯ 3802) to 135 dG (586,118 Ϯ 25,792). NR increased combined kidney weight (29 Ϯ 0.6 g versus 23 Ϯ 1.1 g), whereas decreased GN relative to right kidney weight approached significance in males (26,000 Ϯ 5300 versus 39,000 Ϯ 2800 GN/g) compared with control (C) males and females. NR decreased immunoreactive angiotensin II (Ang II) type 1 receptor (AT1) in the NR kidneys at 78 dG and increased renin at 135 dG. Immunoreactive renin decreased from 78 to 135 dG. Female fetuses had more immunoreactive Ang II type 2 receptor (AT2) than male fetuses at 78 dG and males had more AT1 at 135 dG. The present study demonstrates gender-specific differences in fetal growth and development and in fetal kidney development in pregnancies affected by NR. T he American Kidney Foundation estimates the rates of chronic renal diseases are increasing rapidly, such that 20 million Americans (one in nine adults) have some form of chronic renal disease. Similarly, epidemiologic and animal studies showing a developmental origin for renal dysfunction are also increasing (1-3). This growing body of evidence clearly shows that the kidney is sensitive to perturbations of the fetal environment. Viewed in concert with factors in modern society that may collude to impair fetal nutrition, such as poverty and drug abuse, and clinical conditions, such as hyperemesis gravidarum, anorexia nervosa, and bulimia, it is clear that decreased nutrient delivery to the fetus will affect a large number of pregnancies across socioeconomic strata (4 -6).The acquisition of renal GN is a morphogenic process that reflects sensitivity to a suboptimal intrauterine environment (7,8). Reduced GN has been shown when fetal growth restriction begins early in gestation but not when the insult is restricted to late gestation (9). Interestingly, a reduction in GN following uninephrectomy during fetal life is strongly associated with increased postnatal blood pressure (10,11), whereas adult uninephrectomy is not (12). Factors that affect nephrogenesis during fetal life therefore appear to have a greater impact on blood pressure than the hypertrophic responses induced in the adult to facilitate the maintenance of filtration surface area. In accordance with this perspective, we have recently demonstrated decreased GN associated with hypertension in the male offspring of sheep NR from early to midgestation (7). From these and other studies, it is clear that although the period in which kidney development may be affected is broad, late gestation is not a part of the critical nephrogenic window in large animals such as sheep (7,9,13,14).Previous studi...

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“…The RAS was accepted to have a role in kidney development, with a role in vasculogenesis, branching morphogenesis and development of hypertension in the adult, as the result of a reduction in nephron number during nephrogenesis (7,36).…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Maternal undernutrition and the offspring kidney: from fetal to adult life

Mesquita

Gontijo

Bôer

2010

Braz J Med Biol Res

112

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Role of the renin-angiotensin system in the development of the ureteric bud and renal collecting system

Cited by 31 publications

References 86 publications

Local Fetal Lung Renin-Angiotensin System as a Target to Treat Congenital Diaphragmatic Hernia

Local Fetal Lung Renin-Angiotensin System as a Target to Treat Congenital Diaphragmatic Hernia

Nutrient Restriction Impairs Nephrogenesis in a Gender-Specific Manner in the Ovine Fetus

Maternal undernutrition and the offspring kidney: from fetal to adult life

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