Calcium, cyclic AMP, and MAP kinases: dysregulation in polycystic kidney disease.
Low intracellular calcium, present in untreated polycystic kidney epithelia, results in a proliferative response to cyclic adenosine monophosphate. Treatment with a calcium channel blocker (CCB) caused exacerbation of autosomal dominant polycystic kidney disease in rats. Data regarding use of CCBs in human polycystic kidney disease (PKD) are limited and mixed. Thus, it is premature to extrapolate these findings to human PKD.
Cowley
B D
BD
University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. Ben-Cowley@ouhsc.edu
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000009:adverse effects*; D049109:Cell Proliferation / Q000187:drug effects*; D000075202:Contraindications; D000242:Cyclic AMP / Q000378:metabolism; D018450:Disease Progression; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects; D007690:Polycystic Kidney Diseases / Q000139:chemically induced* / Q000503:physiopathology*; D014700:Verapamil / Q000009:adverse effects*
D002121:Calcium Channel Blockers; D014700:Verapamil; D000242:Cyclic AMP; D002118:Calcium