Evaluation of functional correlation between excitatory amino acids and PGE2 in AV3V mechanisms regulating ADH secretion

(1)清醒大鼠前腹侧第三脑室(AV3V)注射NMDA受体激动剂NMDA或代谢型Glu受体激动剂t-acpd可刺激ADH分泌，并呈剂量依赖性地增加动脉压(AP)和心率(HR)。此外，应用NMDA，但不能使t-acpd升高血浆渗透压、血糖和血细胞计数。预先给予NMDA或t-acpd拮抗剂MK-801或MCPG均可阻断NMDA或t-acpd的上述作用。(2)AV3v应用PGE2可促进AVP的释放和AP、HR的升高。预先应用MK-801或MCPG可阻断PGE2的ADH抑制作用，但不影响其心血管作用。组胺H1受体拮抗剂吡咯胺可抑制PGE2的升压作用，但对PGE2的心血管反应无影响。环磷酸腺苷应用于血管紧张素转换酶时可引起前列腺素E_2样的作用，而预先给予腺苷环化酶抑制剂…更多的SQ22536不影响PGE2对AV3V的作用。(3)静脉输注高渗盐水后，血浆ADH和AP随时间递增。AV3V给药MK-801可选择性地预防ADH反应，而MCPG则无此作用。(4)动脉采血引起的高血压出血使血浆ADH、血管紧张素II、渗透压和血糖升高。AV3V应用MK-801选择性地阻止血浆ADH的反应，而不改变其他变量的反应。脑室注射MK-801或AV3V MCPG不能使出血性ADH反应减弱。(5)在AV3V上应用NO释放剂硝普钠(NP)可促进ADH的分泌，而cGMP不能引起这种现象，而cGMP可促进这种物质的形成。NP诱导的ADH反应不能被阻止，但预先给予鸟苷酸环化酶抑制剂亚甲蓝增强，并被非清除剂血红蛋白消除。(6)用微透析技术从AV3V区收集的间质液中PGE2水平在静脉注射高渗盐水期间或在常压或低血压放血后没有显著变化。较少

(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 … More 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