Opposed actions for nitric oxide (NO) and angiotensin II (Ang II) in vascular contraction and vascular smooth muscle cell proliferation and apoptosis are well documented. In addition, various experimental approaches have shown that NO negatively modulates the renin–angiotensin system by inhibiting angiotensin-converting enzyme (ACE) activity and down-regulating AT1receptors. On the other hand, Ang II and Ang-(1–7) positively stimulate NO synthesis and release. In this review, we analyse the data suggesting a mutual regulation between the renin–angiotensin and the nitric oxide-generating systems, and we propose a homeostatic interplay between both factors aimed at regulating cardiovascular function.