Abstract
Arginine-vasopressin (AVP) is well-known to exert its antidiuretic effect via the vasopressin V2 receptor (V2R), whereas the role of vasopressin V1a receptor (V1aR) in the kidney remains to be clarified. Previously, we reported that the plasma volume and blood pressure are decreased in V1a receptor-deficient (V1aR-KO) mice. In this study, we investigated the role of V1aR in renin-angiotensin system (RAS) using V1aR-KO mice and found that RAS was suppressed in V1aR-KO mice. The V1a receptor is detected at macula densa and granule cells of kidney in control wild mice by the analysis with in situ hybridization and found to be co-localized with the expression of neuronal nitric oxide synthase (nNOS) and cyclooxygenase (COX)-2 in the macula densa (MD) cells. The expression of renin in the granule cell was decreased in V1aR-KO mice, which led to decreased plasma renin level. In addition to the decreased renin expression, the expression of renin stimulators such as neuronal nitric oxide synthase (nNOS) and cyclooxygenase (COX)-2 in the macula densa (MD) cells, where V1aR was specifically expressed, was decreased in V1aR-KO mice. These data indicate that AVP regulates body fluid homeostasis via the V1aR in the MD cell by activating RAS. The disruption of V1aR led to decreased plasma volume and hypotension. [J Physiol Sci. 2008;58 Suppl:S21]
