Arginine vasopressin (AVP) は血管平滑筋細胞のV1受容体を介して、強い収縮作用を発揮し、血管昇圧反応を示すことはよく知られている。しかし、AVPが最も顕著な作用を発揮するのは腎集合管のV2受容体を介する抗利尿作用である。従って、AVPが高血圧の発症・維持には果たす役割については、いまだに十分に解明されていない。我々は、実験的高血圧モデルを用いて、腎のV2受容体の変化について検討してきた。ここでは、我々の成績を紹介して、実験的高血圧の分野での概要を示すとともに、本態性高血圧におけるAVPの役割についての最近の知見をまとめた。Arginine vasopressin (AVP) interacts with at least two types of receptors, classified according to their second messengers. The vasoconstrictive effect on systemic arteries is mediated throgh V1 receptors. The antidiuretic effect of AVP is mediated by V2 receptors located mainly in the renal collecting ducts. V1 receptors are not affected by physiological dose of AVP blood pressure control, so the biological significance of AVP in blood pressure control is unknown. In the field of hypertension research, various hypertension animal models have been used. Spontaneouslyhypertensive rats (SHR), DOCA-salt hyperteisive rats, Dahl salt-sensitive or Dahl saltresistant rats. SHR are often used as a model of human essential hypertension, whereas the DOCA model is considered to be a model of volume dependent hypertension. Relationship between AVP and regulation of blood pressure was reviewed
