| First Author | Nomura K | Year | 2019 |
| Journal | Neuron | Volume | 101 |
| Issue | 1 | Pages | 60-75.e6 |
| PubMed ID | 30503172 | Mgi Jnum | J:268972 |
| Mgi Id | MGI:6268957 | Doi | 10.1016/j.neuron.2018.11.017 |
| Citation | Nomura K, et al. (2018) [Na(+)] Increases in Body Fluids Sensed by Central Nax Induce Sympathetically Mediated Blood Pressure Elevations via H(+)-Dependent Activation of ASIC1a. Neuron |
| abstractText | Increases in sodium concentrations ([Na(+)]) in body fluids elevate blood pressure (BP) by enhancing sympathetic nerve activity (SNA). However, the mechanisms by which information on increased [Na(+)] is translated to SNA have not yet been elucidated. We herein reveal that sympathetic activation leading to BP increases is not induced by mandatory high salt intakes or the intraperitoneal/intracerebroventricular infusions of hypertonic NaCl solutions in Nax-knockout mice in contrast to wild-type mice. We identify Nax channels expressed in specific glial cells in the organum vasculosum lamina terminalis (OVLT) as the sensors detecting increases in [Na(+)] in body fluids and show that OVLT neurons projecting to the paraventricular nucleus (PVN) are activated via acid-sensing ion channel 1a (ASIC1a) by H(+) ions exported from Nax-positive glial cells. The present results provide an insight into the neurogenic mechanisms responsible for salt-induced BP elevations. |
