Inhibition of the renin-angiotensin-system (RAS) leads to a compensatory increase of renin-producing cells in the kidneys, which is brought about by a reversible phenotype switch of renin-precursor cells into renin-expressing cells. Such a recruitment of additional renin-expressing cells occurs typically along the preglomerular vasculature but also in the periglomerular interstitium such as in mice lacking connexin 40. The cellular mechanisms triggering the reversible phenotype switch are mainly unknown. Since endothelial autacoids including nitric oxide are known to (in)directly modulate the function of renin-secreting cells in the kidney, this study aimed to assess the role nitric oxide for the phenotype switch of renin-expressing cells in animals with an inhibited RAS, such as in mice either lacking angiotensin II-AT1a receptors or receiving the ACE-inhibitor enalapril. Systemic inhibition of nitric oxide formation by treatment with the NOS-inhibitor L-NAME strongly reduced the increased numbers of renin-expressing cells in the beforementioned mouse strains. Notably L-NAME treatment failed to reduce the number of renin-expressing cells in eNOS deficient mice treated with enalapril. These findings suggest that it is mainly eNOS derived nitric oxide that is relevant for the recruitment of renin-expressing cells. In all treatment groups the number of renin-expressing cells was inversely related to the blood pressure values. Since L-NAME treatment clearly increased blood pressure in all animals with the exception of eNOS deficient mice, we suppose that the inhibition of renin cell recruitment by systemic NO blockade is due to blood pressure changes rather than to specific intracellular NO mediated signaling cascades. Our findings therefore support the notion that the blood pressure in the renal preglomerular vascular tree is probably the master regulator of renin cell recruitment.