Dietary salt intake controls epithelial Na+ channel (ENaC)-mediated Na+ reabsorption in the
distal nephron by affecting status of the renin-angiotensin-aldosterone system (RAAS).
Whereas regulation of ENaC by aldosterone is generally accepted, little is known about
whether other components of RAAS, such as angiotensin II (Ang II), have nonredundant to
aldosterone-stimulatory actions on ENaC. We combined patch clamp electrophysiology and
immunohistochemistry in freshly isolated split-opened distal nephrons of mice to determine …