دورية أكاديمية

Role of the renin-angiotensin system in kidney development and programming of adult blood pressure

التفاصيل البيبلوغرافية
العنوان: Role of the renin-angiotensin system in kidney development and programming of adult blood pressure
المؤلفون: Almeida, Lucas F., Tofteng, Signe S., Madsen, Kirsten, Jensen, Boye L.
المصدر: Almeida , L F , Tofteng , S S , Madsen , K & Jensen , B L 2020 , ' Role of the renin-angiotensin system in kidney development and programming of adult blood pressure ' , Clinical Science , vol. 134 , no. 6 , pp. 641-656 . https://doi.org/10.1042/CS20190765Test
سنة النشر: 2020
المجموعة: University of Southern Denmark: Research Output / Syddansk Universitet
مصطلحات موضوعية: development, hypertension, kidney, renin, Blood Pressure, Renin/metabolism, Vascular Endothelial Growth Factor A/genetics, Hypertension/genetics, Humans, Kidney/growth & development, Animals, Renin-Angiotensin System, Angiotensins/metabolism
الوصف: Adverse events during fetal life such as insufficient protein intake or elevated transfer of glucocorticoid to the fetus may impact cardiovascular and metabolic health later in adult life and are associated with increased incidence of type 2 diabetes, ischemic heart disease and hypertension. Several adverse factors converge and suppress the fetal renin-angiotensin-aldosterone system (RAAS). The aim of this review is to summarize data on the significance of RAAS for kidney development and adult hypertension. Genetic inactivation of RAAS in rodents at any step from angiotensinogen to angiotensin II (ANGII) type 1 receptor (AT1) receptors or pharmacologic inhibition leads to complex developmental injury to the kidneys that has also been observed in human case reports. Deletion of the 'protective' arm of RAAS, angiotensin converting enzyme (ACE) 2 (ACE-2) and G-protein coupled receptor for Angiotensin 1-7 (Mas) receptor does not reproduce the AT1 phenotype. The changes comprise fewer glomeruli, thinner cortex, dilated tubules, thicker arterioles and arteries, lack of vascular bundles, papillary atrophy, shorter capillary length and volume in cortex and medulla. Altered activity of systemic and local regulators of fetal-perinatal RAAS such as vitamin D and cyclooxygenase (COX)/prostaglandins are associated with similar injuries. ANGII-AT1 interaction drives podocyte and epithelial cell formation of vascular growth factors, notably vascular endothelial growth factor (VEGF) and angiopoietins (Angpts), which support late stages of glomerular and cortical capillary growth and medullary vascular bundle formation and patterning. RAAS-induced injury is associated with lower glomerular filtration rate (GFR), lower renal plasma flow, kidney fibrosis, up-regulation of sodium transporters, impaired sodium excretion and salt-sensitive hypertension. The renal component and salt sensitivity of programmed hypertension may impact dietary counseling and choice of pharmacological intervention to treat hypertension.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: https://portal.findresearcher.sdu.dk/da/publications/f3f63c91-49fb-4052-acfc-6239aef435d3Test
DOI: 10.1042/CS20190765
الإتاحة: https://doi.org/10.1042/CS20190765Test
https://portal.findresearcher.sdu.dk/da/publications/f3f63c91-49fb-4052-acfc-6239aef435d3Test
حقوق: info:eu-repo/semantics/closedAccess
رقم الانضمام: edsbas.4D5D7F89
قاعدة البيانات: BASE