Cardiovascular Drugs and Therapy

, Volume 10, Issue 5, pp 511–518

Pathologic consequences of increased angiotensin II activity

Authors

  • Carlos M. Ferrario
    • Hypertension CenterBowman Gray/Baptist Hospital Medical Center of Wake Forest University
  • John M. Flack
    • Hypertension CenterBowman Gray/Baptist Hospital Medical Center of Wake Forest University
Review Articles

DOI: 10.1007/BF00050990

Cite this article as:
Ferrario, C.M. & Flack, J.M. Cardiovasc Drug Ther (1996) 10: 511. doi:10.1007/BF00050990

Summary

Advances in molecular medicine and pharmacology have allowed clinicians to critically reassess the reninangiotensin system. Angiotensin II (AII) participates in the control of cardiovascular function and electrolyte balance, and plays a part in the regulation of cellular oncogenes and the expression of growth factors. The expression of the proteins of the renin-angiotensin system in organs other than the kidneys suggests that these diverse actions are associated with the peptide in the local environment. Tissue reninangiotensin activity has prompted the investigation of alternate pathways for the production of AII and characterization of novel forms of angiotensin peptides that counteract the vasoconstrictor and proliferative actions of AII. The heptapeptide angiotensin-(1–7) appears to be critically involved in regulating the angiotensinogen activity of AII through stimulation of vasodilator prostaglandins and release of nitric oxide. Study in this area has been accelerated by the identification of receptors that convey the actions of angiotensin peptides at the cellular level and the pharmacologic characterization of agents that inhibit the ability of AII to bind to target receptors. The introduction of a new class of orally active AII-receptor blockers has provided a specific test of the role of AII in the development of essential hypertension and the potential for improved therapy for hypertension and cardiac and vascular sequelae.

Key Words

renin-angiotensin systemangiotensin IIhypertensionAT1 receptorAT2 receptorangiotensin-receptor blockerlosartan

Copyright information

© Kluwer Academic Publishers 1996