Renal enlargement in polycystic kidney disease (PKD) is caused by the proliferation of
mural epithelial cells and transepithelial fluid secretion into the cavities of innumerable cysts.
Arginine vasopressin (AVP) stimulates the proliferation of human PKD cells in vitro via cAMP-
dependent activation of the B-Raf/MEK (MAPK/ERK kinase/extracellular signal–regulated
kinase (ERK) pathway. ERK activity is elevated in cells that line the cysts in animals with
PKD, and AVP receptor antagonists reduce ERK activity and halt disease progression. For …