|Budget Amount *help
¥3,400,000 (Direct Cost : ¥3,400,000)
Fiscal Year 2004 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 2003 : ¥1,400,000 (Direct Cost : ¥1,400,000)
Fiscal Year 2002 : ¥1,300,000 (Direct Cost : ¥1,300,000)
(1)In conscious rats, administrations of a NMDA receptor agonist NMDA or a metabotropic Glu receptor agonist t-ACPD into the anteroventral third ventricle (AV3V) stimulated ADH secretion and increased arterial pressure(AP) and heart rate(HR) in a dose-related manner. Moreover, the applications of NMDA, but not t-ACPD raised plasma osmolalily, glucose and hematocrte. All the effects of NMDA or t-ACPD, excepting the tachycardiac actions, were blocked by pre-administering respective antagonists MK-801 or MCPG.
(2)AV3V applications of PGE2 produced facilitation of AVP release and elevations of AP and HR. Pre-applications of MK-801 or MCPG blocked the ADH-reteasing effect of PGE2, without affecting its cardiovascular actions. The pressor action of PGE2 was inhibited by a histamine H1 receptor antagonist pyrilamine that exerted no effect on the cardiovascular responses to PGE2. Cyclic AMP caused PGE2-like actions when applied to AVSV, whereas pre-administrations of an adenyl cyclase inhibitor
SQ22536 affected none of the the effects of PGE2 administered to AV3V.
(3)Intravenous infusions of hypertonic saline raised plasma ADH and AP progressively with time. The ADH response was selectively prevented by AV3V administrations of MK-801, whereas those of MCPG were without effect.
(4)Hypertensive bleeding, but not normotensive one, provoked by withdrawing arterial blood augmented plasma ADH, angiotensin II, osmolality and glucose. AV3V applications of MK-801 prevented the response of plasma ADH selectively, without changing those of the other variables. Such attenuation in the hemorrhagic ADH response was not produced by intraventricular applications of MK-801 or AV3V sdministrations of MCPG.
(5)Applications of a nitric oxide (NO)-releasing agent nitroprusside(NP) to AV3V facilitated ADH secretion, whereas the phenomenon was not evoked by the treatment with cGMP, a substance of which formation can be enhanced by NO. The NP-induced ADH response was not prevented, but intensified by pre-administrations of a guanyl cyclase inhibitor methylene blue, and abolished by those of a NO-scavenger hemoglobin.
(6)PGE2 levels in the interstitial fluid collected from AV3V area using a microdyalysis technique did not change significantly during intravenous infusions of hypertonic saline or after normotensive or hypotensive bleedings. Less