抄録
We have previously proposed a role of NMDA receptors in the anteroventral third ventricular region (AV3V) in a hypovolemic VP secretion, on the basis of the potency of AV3V infusion of its antagonist (MK) to inhibit the plasma VP response to hemorrhage. However, as it causes two other stimuli for VP release, the rises in plasma (p) osmolality (Osm) and angiotensin (ANG) II, it is possible that the MK treatment might have blunted the response by interfering these events. Moreover, it could be suspected that MK applied to the AV3V, a juxta-ventricular area, might have diffused into the ventricular space to produce the effect via actions on remote regions. The aim of this study was to further explore validity of the view by examining those problems. In conscious and unrestrained rats, normotensive (H1) and hypotensive hemorrhages (H2) were induced successively by removing arterial blood twice at a 10-min interval. The H2, but not H1, augmented VP, Osm, glucose and ANG II in plasma, and reduced its K+. PNa+ and heart rate were not changed. MK administered into the AV3V 15 min preceding H1 was verified to block the VP response to H2, whereas it did not affect the responses of pANG II, pOsm, glucose, blood pressure or other variables. When infused into the cerebral ventricle, MK did not influence the VP response. Thus, the present results provide further support for our proposal that NMDA receptors in the AV3V may operate to mediate VP secretion in the state with hypotensive hypovolemia. [Jpn J Physiol 54 Suppl:S219 (2004)]
