Nax-deficient mice show normal vasopressin response to dehydration

In dehydrated animals, the antidiuretic hormone vasopressin (VP) is released from the nerve terminals of magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) into the systemic circulation at the posterior pituitary. Increases in sodium (Na+)-level and osmolality in body fluids upon dehydration are reportedly sensed by a Na+-sensor and/or an osmosensor, respectively. However, it is still unknown whether both are involved in the regulation of production and/or release of VP. Nax is the cerebral Na+-level sensor and Nax-knockout mice do not stop ingesting salt even when dehydrated. Here we examined VP production/release in Nax-knockout mice, and found that they are normal in the VP response to dehydration or intraperitoneal-administration with hypertonic saline. In situ hybridization using an intron-specific probe showed that VP gene expression in the SON did not differ from wild-type mice when dehydrated. Also, there was no significant difference in the activity of subfornical organ neurons projecting to the SON between the two genotypes when stimulated by water deprivation. Furthermore, Nax-knockout mice showed a normal response in urine excretion to dehydration. All these results indicate that the information of Na+-level increase detected by Nax does not contribute to the control of VP production/release.