Angiotensin II and nitric oxide: a question of balance

The vasoconstrictor peptide angiotensin II (Ang II) and the endogenous vaso dilator nitric oxide (NO) have many antagonistic effects, as well as influe ncing each other's production and functioning. In the short-term, Ang II st imulates NO release, thus modulating the vasoconstrictor actions of the pep tide. In the long-term, Ang II influences the expression of all three NO sy nthase (NOS) isoforms, while NO downregulates the Ang II Type I (AT(1)) rec eptor, contributing to the protective role of NO in the vasculature. Within the cardiovascular system, Ang II and NO also have antagonistic effects on vascular remodeling and apoptosis. In the kidney, the distribution of the NOS isoforms coincides with the sites of the components of the renin-angiot ensin system. NO influences renin secretion from the: kidney, and NO-Ang II interactions are important in the control of glomerular and tubular functi on. In the adrenal gland, NO has been shown to affect Ang II-induced aldost erone synthesis, while in the brain NO appears to influence Ang II-induced drinking behavior, although conflicting data have been reported. In this re view, we focus on the diverse ways in which Ang II and NO interact, and on the importance of maintaining a balance between these two important mediato rs. (C) 1999 Elsevier Science B.V. All rights reserved.