Angiotensin II-nitric oxide interaction in glomerular arterioles

Clin Exp Pharmacol Physiol. 2005 May-Jun;32(5-6):410-4. doi: 10.1111/j.1440-1681.2005.04203.x.

Abstract

1. Resistance changes of the afferent and efferent arterioles determine blood flow and filtration rate in the kidney. The tone of both vessels results from the influence of nerves and humoral and paracrine factors, through a balance of constrictor and dilator systems. Angiotensin (Ang) II and nitric oxide (NO) are important factors determining vascular tone. 2. In the present review, we show that, in addition to the basal production of NO, a specific and significant AngII-induced release of NO occurs in glomerular arterioles. Data from investigations of arteriolar contraction, as well as from fluorescence measurements of NO, in the presence of selective angiotensin AT(1) and AT(2) receptor antagonists indicate an AT(1) receptor-stimulated release of NO in afferent arterioles. 3. The AngII-induced liberation of NO could prevent glomerular arterioles from a marked constriction, particularly in situations of high AngII levels in the kidney.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin II / metabolism*
  • Angiotensin II / pharmacology
  • Animals
  • Arterioles / drug effects
  • Arterioles / metabolism
  • Dose-Response Relationship, Drug
  • Humans
  • Kidney Glomerulus / blood supply*
  • Kidney Glomerulus / drug effects
  • Kidney Glomerulus / metabolism*
  • Nitric Oxide / metabolism*

Substances

  • Angiotensin II
  • Nitric Oxide