A defect in vasopressin secretion in autosomal dominant polycystic kidney disease.

A nephrogenic defect in urine concentration is well established in patients with polycystic kidney disease, but Ho et al. report a defect in the increase of plasma vasopressin in response to dehydration. On a cellular level, transient receptor potential channels responsible for osmoperception could interact with TRPPs encoded by the polycystic genes PKD1 and PKD2.