Etiology of angiogenesis inhibition-related hypertension

Curr Opin Pharmacol. 2015 Apr:21:7-13. doi: 10.1016/j.coph.2014.11.010. Epub 2014 Dec 12.

Abstract

Angiogenesis inhibition, targeting vascular endothelial growth factor (VEGF) or its receptors, is an established treatment for solid tumors. A common side effect of this treatment is the development of sometimes severe hypertension. This hypertension is associated with a decrease in nitric oxide production, activation of the endothelin-signaling pathway and renin suppression. The mechanism underlying activation of the endothelin-signaling pathway is not fully understood. Both activation of endothelial cells and disinhibition of the VEGF-induced suppression of endothelin production by endothelial cells may be involved. The development of hypertension can be a reason to discontinue the angiogenesis inhibitor, thereby compromising anticancer treatment, but possibly is also a biomarker for a favorable antitumor response.

Publication types

  • Review

MeSH terms

  • Angiogenesis Inhibitors / adverse effects*
  • Animals
  • Endothelin-1 / metabolism
  • Humans
  • Hypertension / chemically induced*
  • Hypertension / metabolism*
  • Kidney / drug effects
  • Kidney / metabolism
  • Kidney / physiology
  • Nitric Oxide / metabolism
  • Renin-Angiotensin System
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Angiogenesis Inhibitors
  • Endothelin-1
  • Vascular Endothelial Growth Factor A
  • Nitric Oxide