Angiotensin receptors in the kidney and vasculature in hypertension and kidney disease.

Journal Article (Journal Article;Review)

Kidney disease, blood pressure determination, hypertension pathogenesis, and the renin-angiotensin system (RAS) are inextricably linked. Hence, understanding the RAS is pivotal to unraveling the pathophysiology of hypertension and the determinants to maintaining normal blood pressure. The RAS has been the subject of intense investigation for over a century. Moreover, medications that block the RAS are mainstay therapies in clinical medicine and have been shown to reduce morbidity and mortality in patients with diabetes, cardiovascular, and kidney diseases. The main effector peptide of the RAS is the interaction of the octapeptide- Ang II with its receptor. The type 1 angiotensin receptor (AT1R) is the effector receptor for Ang II. These G protein-coupled receptors (GPCRs) are ubiquitously expressed in a variety of cell lineages and tissues relevant to cardiovascular disease throughout the body. The advent of cell specific deletion of genes using Cre LoxP technology in mice has allowed for the identification of discreet actions of AT1Rs in blood pressure control and kidney disease. The kidney is one of the major targets of the RAS, which is responsible in maintaining fluid, electrolyte balance, and blood pressure. In this review we will discuss the role of AT1Rs in the kidney, vasculature, and immune cells and address their effects on hypertension and kidney disease.

Full Text

Duke Authors

Cited Authors

  • Rianto, F; Hoang, T; Revoori, R; Sparks, MA

Published Date

  • June 1, 2021

Published In

Volume / Issue

  • 529 /

Start / End Page

  • 111259 -

PubMed ID

  • 33781840

Electronic International Standard Serial Number (EISSN)

  • 1872-8057

Digital Object Identifier (DOI)

  • 10.1016/j.mce.2021.111259


  • eng

Conference Location

  • Ireland