Abstract
Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT1 receptors and NADPH oxidase, and lower expression of AT2, Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension.
Highlights
Publisher’s Note: MDPI stays neutralThe renin-angiotensin system (RAS) is a very complex system involving many peptides and receptors
One of such peptides is angiotensin I (Ang I) that result from angiotensinogen cleavage and is transformed into angiotensin II (Ang II) by the angiotensin-converting enzyme (ACE)
The angiotensin converting enzyme 2 (ACE2)/Ang 1–7 and alamandine axis leads to an increase of nitric oxide (NO) bioavailability and a decrease of oxidative stress, through inhibition of nicotinamide with regard to jurisdictional claims in published maps and institutional affiliations
Summary
Publisher’s Note: MDPI stays neutralThe renin-angiotensin system (RAS) is a very complex system involving many peptides and receptors. The classical RAS axis (renin/ACE/Ang II/AT1 receptor) is known to promote vasoconstriction and to increase oxidative stress, fibrosis, and inflammation (through activation of AT1 receptors). These Ang II-AT1 receptor effects are counteracted by a non-classical RAS axis, formed by other peptides, enzymes and receptors [1,2,3]. The peptide angiotensin-(1–7) (Ang 1–7), that is mainly formed directly from Ang II by angiotensin converting enzyme 2 (ACE2), and the peptide alamandine. These peptides bind, respectively, to the Mas receptor and/or Mas-related G protein-coupled receptor D (MrgD). The ACE2/Ang 1–7 and alamandine axis leads to an increase of nitric oxide (NO) bioavailability and a decrease of oxidative stress, through inhibition of nicotinamide with regard to jurisdictional claims in published maps and institutional affiliations
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