抄録
It is well known that activation of glutamatergic NMDA receptors in brain areas such as the cerebellum stimulates syntheses of nitric oxide (NO) and cGMP, leading to cooperation in forming synaptic plasticity or promoting neurotransmission. However, existence of such action modes in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic function, is not certain. The aim of this study was to address the issue by experiments in conscious rats. Local infusion of NMDA to the AV3V caused dose-related rises of plasma ADH (VP), osmolality, glucose and arterial pressure (AP). These phenomena were blocked by preadministering its antagonist MK-801 (MK). AV3V injections of the NO substrate L-Arg and a NO donor sodium nitroprusside (SNP) were also potent to provoke those phenomena. The effects of L-Arg and SNP were inhibited, respectively, by the pretreatments with a NO synthase inhibitor L-NAME (NAME) and a NO scavenger hemoglobin. However, plasma osmolality did not increase after the AV3V infusions of the NO-producing drugs, and the infusion of a cGMP analogue did not elevate plasma VP. Moreover, none of the NMDA-evoked responses were not blunted by preapplicating NAME. Furthermore, the VP response to i.v. load of hypertonic NaCl was prevented by the AV3V injection of MK, but not by that of NAME. These results suggest that, despite its potent local actions, NO may not play mediatory or cooperative roles when AV3V NMDA receptors may operate to activate autonomic functions. [Jpn J Physiol 55 Suppl:S206 (2005)]
