Intrarenal angiotensin II and its contribution to the genesis of chronic hypertension

Curr Opin Pharmacol. 2011 Apr;11(2):180-6. doi: 10.1016/j.coph.2011.01.009. Epub 2011 Feb 19.

Abstract

The increased activity of intrarenal renin-angiotensin system (RAS) in a setting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, proliferation, fibrosis and renal injury. Increases in intrarenal and interstitial angiotensin (Ang) II levels are due to increased AT(1) receptor mediated Ang II uptake and stimulation of renal angiotensinogen (AGT) mRNA and protein expression. Augmented proximal tubule AGT production increases tubular AGT secretion and spillover of AGT into the distal nephron and urine. Increased renin formation by principal cells of the collecting ducts forms Ang I from AGT thus increasing Ang II. The catalytic actions of renin and prorenin are enhanced by prorenin receptors (PRRs) on the intercalated cells. The resultant increased intrarenal Ang II levels contribute to the genesis of chronic hypertension.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin II / physiology*
  • Angiotensinogen / physiology
  • Animals
  • Chronic Disease
  • Humans
  • Hypertension / etiology*
  • Kidney / physiology*
  • Kidney Tubules, Collecting / physiology
  • Receptors, Cell Surface / physiology
  • Renin / physiology

Substances

  • Receptors, Cell Surface
  • prorenin receptor
  • Angiotensinogen
  • Angiotensin II
  • Renin