Effects of early overnutrition on the renal response to Ang II and expression of RAAS components in rat renal tissue

Nutr Metab Cardiovasc Dis. 2017 Oct;27(10):930-937. doi: 10.1016/j.numecd.2017.06.019. Epub 2017 Jul 8.

Abstract

Background and aims: The aim of this study was to analyze the effects of early overnutrition (EON) on the expression of the renin angiotensin aldosterone system (RAAS) components in renal cortex, renal arteries and renal perivascular adipose tissue (PVAT), as well as the vascular response of renal arteries to Angiotensin II (Ang II).

Methods and results: On birth day litters were adjusted to twelve (L12-control) or three (L3-overfed) pups per mother. Half of the animals were sacrificed at weaning (21 days old) and the other half at 5 months of age. Ang II-induced vasoconstriction of renal artery segments increased in young overfed rats and decreased in adult overfed rats. EON decreased the gene expression of angiotensinogen (Agt), Ang II receptors AT1 and AT2 and eNOS in renal arteries of young rats, while it increased the mRNA levels of AT-2 and ET-1 in adult rats. In renal PVAT EON up-regulated the gene expression of COX-2 and TNF-α in young rats and the mRNA levels of renin receptor both in young and in adult rats. On the contrary, Ang II receptors mRNA levels were downregulated at both ages. Renal cortex of overfed rats showed increased gene expression of Agt in adult rats and of AT1 in young rats. However the mRNA levels of AT1 were decreased in the renal cortex of overfed adult rats.

Conclusion: EON is associated with alterations in the vascular response of renal arteries to Ang II and changes in the gene expression of RAAS components in renal tissue.

Keywords: Angiotensin II; Early overnutrition; Perivascular adipose tissue; Rat; Renal arteries.

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Adipose Tissue / physiopathology
  • Age Factors
  • Angiotensin II / pharmacology*
  • Animal Nutritional Physiological Phenomena
  • Animals
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation
  • Kidney / blood supply*
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • Nutritional Status
  • Overnutrition / genetics
  • Overnutrition / metabolism*
  • Overnutrition / physiopathology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats, Sprague-Dawley
  • Receptor, Angiotensin, Type 1 / genetics
  • Receptor, Angiotensin, Type 1 / metabolism
  • Receptor, Angiotensin, Type 2 / genetics
  • Receptor, Angiotensin, Type 2 / metabolism
  • Renal Artery / drug effects*
  • Renal Artery / metabolism
  • Renal Artery / physiopathology
  • Renin-Angiotensin System / drug effects*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Vasoconstriction / drug effects*
  • Vasoconstrictor Agents / pharmacology*

Substances

  • RNA, Messenger
  • Receptor, Angiotensin, Type 1
  • Receptor, Angiotensin, Type 2
  • Tumor Necrosis Factor-alpha
  • Vasoconstrictor Agents
  • Angiotensin II
  • Nitric Oxide Synthase Type III
  • Nos3 protein, rat
  • Cyclooxygenase 2
  • Ptgs2 protein, rat