The field of cGMP/cGKII-mediated mechanisms regarding kidney function is rather unexplored. ANP, as the major upstream regulator of cGKII, is known to cause diuresis and natriuresis by renal vascular as well as direct tubular effects. The collecting duct (CD) is thought to be the main target site of ANP in the kidney; an inhibition of Na+- reabsorption was shown for outer and inner medullary CD [1–3]. In contrast, the effect of ANP on fluid reabsorption in CD is discussed very controversially. Short-term regulation of Aquaporin 2 (AQP2), the predominant apical water channel in the CD, occurs mainly via membrane insertion/excision. Stimulation as well as inhibition of AQP2-trafficking upon ANP-administration have been reported [4, 5]. However, the downstream effectors of ANP regarding fluid- and ion-absorption have not been elucidated so far.