Abstract
Vitamin D (Vit.D) is involved in cellular proliferation and differentiation and regulation of the renin gene, which are important aspects of nephrogenesis and quiescence of renal health in adulthood. This study evaluated the angiogenic mechanisms involved in long term renal disturbances induced by Vit.D deficiency persistent in adulthood in rats. First-generation male Hannover offspring from mothers fed either a control diet (control group, CG) or Vit.D-deficient diet (Vit.D- group) were evaluated. Systolic blood pressure (SBP) was measured monthly during the first 6 months after birth, and blood and urine samples were collected to evaluate renal function. Nitric oxide (NO), angiotensin II (ANGII), parathyroid hormone (PTH), calcium, and Vit.D were measured. The kidneys were then removed for morphometric, NO, immunohistochemical, and Western blot studies. We evaluated the expression of vascular growth factor (VEGF) and angiopoietins 1 and 2 and their receptors since this intrinsic renal axis is responsible for endothelial quiescence. Compared to CG, the Vit.D- group presented higher SBP, ANG II plasma levels, renin expression, and AT1 receptor expression levels. Capillary rarefaction was observed, as well as an imbalance between pro- and anti-angiogenic factors. Collectively, the present findings support the role of Vit.D for maintaining the integrity of renal microcirculation.
Highlights
Changes in the intrauterine environment provoked by pharmacologic or genetic deletion of components of the renin-angiotensin system (RAS), maternal dietary manipulation, and sleep restriction during development result in cardiovascular, renal, and metabolic disorders that persist into adulthood in the resulting offspring [1,2,3,4]
We have previously demonstrated the importance of an intact Renin-Angiotensin System (RAS) cascade during kidney development using models of pharmacological inhibition and Vit.D deficiency [3,19,20]
The hypothesis of the present study was that Vit.D deficiency during the kidney development the renal development period are essential to a normal development and maintenance of the renal can cause dysfunctional renal microcirculation due to a lack of cell differentiation by upregulating microcirculation
Summary
Changes in the intrauterine environment provoked by pharmacologic or genetic deletion of components of the renin-angiotensin system (RAS), maternal dietary manipulation, and sleep restriction during development result in cardiovascular, renal, and metabolic disorders that persist into adulthood in the resulting offspring [1,2,3,4]. This predisposition towards adult disease is known as developmental origins of health and disease (DOHaD) or developmental programming [5,6]. Vit.D has pleiotropic effects that extend beyond its traditional role in calcium homeostasis [10]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
