テイphカ デノ ジン ニョウサイカン ナイ バソプレシン V1a ト V2 ジュヨウタイ ノ ソウゴ サヨウ ノ ケントウ

Arginine-vasopressin (AVP) plays a key role in the urine concentration mechanism via the vasopressin V2 receptor (V2R) and aquaporin 2 (AQP2) in the kidney. It is well known that V2R is localized on the basolateral side and the V1a receptor (V1aR) is distributed on the luminal side of the collecting ducts. Previously, we have reported an increase of V1aR mRNA and decrease of V2R mRNA in the collecting duct under chronic metabolic acidosis. However, the regulatory mechanism of V2R in acidic conditions has not been determined yet. The purpose of the present study is to investigate the regulatory mechanism of V2R and the effect of V1aR stimulation on V2R expression under acidic conditions