Role of vasopressin antagonists

Clinical Journal of the American Society of Nephrology : CJASN
Vicente E Torres

Abstract

Alterations in intracellular calcium homeostasis and cyclic adenosine 3',5'-phosphate likely underlie the increased cell proliferation and fluid secretion in polycystic kidney disease. Hormone receptors that affect cyclic adenosine 3',5'-phosphate and are preferentially expressed in affected tissues are logical treatment targets. There is a sound rationale for considering the arginine vasopressin V2 receptor as a target. The arginine vasopressin V2 receptor antagonists OPC-31260 and tolvaptan inhibit the development of polycystic kidney disease in cpk mice and in three animal orthologs to human autosomal recessive polycystic kidney disease (PCK rat), autosomal dominant polycystic kidney disease (Pkd2-/WS25 mice), and nephronophthisis(pcy mouse). PCK rats that are homozygous for an arginine vasopressin mutation and lack circulating vasopressin are markedly protected. Administration of V2 receptor agonist 1-deamino-8-D-arginine vasopressin to these animals completely recovers the cystic phenotype. Administration of 1-deamino-8-D-arginine vasopressin to PCK rats with normal arginine vasopressin aggravates the disease. Suppression of arginine vasopressin release by high water intake is protective. V2 receptor antagonists may have a...Continue Reading

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