兔室旁核对血量扩张引起促纳排泄与利尿的作用

在室旁核 (PVN)假损毁兔与PVN损毁兔血量扩张 (VE)引起尿流量增加 ,峰值分别为 0 5 9± 0 0 9与0 3 1± 0 0 3ml/min (P <0 0 1) ,排钠量增加峰值分别为 66 76± 6 74与 3 6 0 5± 3 4 4μmol/min (P <0 0 1) ,而在PVN假损毁兔与PVN完好兔对VE的反应无显著差别 (P >0 0 5 ) ,表明PVN损伤可明显减弱VE引起的促钠排泄与利尿效应。颈迷走神经切断并不能改变PVN损伤的上述作用。双侧肾神经切断兔损毁PVN对VE引起促钠排泄效应无显著影响 ,但显著减弱其利尿效应 (P <0 0 2 )。PVN损毁对VE时肾小球滤过率 (GFR)与肾血浆流量 (RPF)无显著影响。结果表明PVN参与VE通过迷走传入神经引起促钠排泄与利尿反应的调节 ,而肾交感传出神经参与其中促钠排泄的作用     

兔脊髓α受体对血量扩张引起肾交感神经活动抑制和促钠排泄的作用

在窦主动脉去神经麻醉兔观察阻断脊髓α受体对血量扩张引起肾交感神经活动（RSNA）抑制和促钠排泄反应的影响。兔脊髓蛛网膜下腔注射a肾上腺素能受体阻断剂酚妥拉明与人工脑脊液后,血量扩张引起RSNA抑制分别为（－25．4±5．4）％与（－42．5±5.2）％（P＜0.05）;兔脊髓蛛网膜下腔注射α1受体阻断剂哌唑嗪与人工脑脊液后血量扩张引起RSNA抑制分别为（－29．3±6.1）％与（－42．5±5.2）％（P＜005）。结果表明,阻断脊髓α受体或α1受体均可减弱血量扩张引起RSNA抑制。脊髓注射哌唑嗪后血量扩张引起促钠排泄与利尿反应也显著减弱（P＜005）。     

大鼠脑胆碱能系统对血量扩张引起利尿与尿钠排泄...

The role of brain cholinergic system on diuresis and natriuresis induced by volume expansion was studied in conscious rats. In a series of experiments, the diuretic, natriuretic and kaliuretic responses induced by volume expansion were compared in three groups of conscious rats pretreated respectively with intracerebroventricular (icv) injection of artificial cerebrospinal fluid (ACSF), atropine and hexamethonium. The natriuretic, kaliuretic and diuretic responses induced by volume expansion were much less in the animals with icv injection of atropine than in the control group with injection of ACSF (P less than 0.01). While the group pretreated with icv injection of hexamethonium showed no significant decrease in these responses of volume expansion than that of the control (P greater than 0.05). Volume expansion produced no change in insulin and PAH clearance in both the atropine and the ACSF group. Thus the atropine suppressed diuresis, natriuresis and kaliuresis are independent of changes in GFR and RPF. It is inferred from the results of the present investigation that volume expansion induced diuresis and natriuresis appear to be due to inhibition of water and sodium reabsorption in the renal tubules and regulated by certain brain cholinergic system.     

兔室旁核－脊髓径路对血量扩张引起肾交感神经活动抑制的作用

在室旁核（ＰＶＮ）完好或ＰＶＮ注射抗坏血酸的双侧窦主动脉去神经的麻醉兔,血量扩张引起肾交感神经活动（ＲＳＮＡ）抑制均约４８％。然而在红藻氨酸损毁ＰＶＮ后的３—４ｈ和３—４ｄ,这种ＲＳＮＡ抑制分别减弱到－２８．０±４．５％和－２５．７±４．１％（Ｐ＜０．０５）,同时其抑制时程也显著缩短（Ｐ＜０．０１）。此ＲＳＮＡ抑制也可被脊髓Ｔ１０—Ｔ１２节段蛛网膜下腔注射血管升压素能Ｖ１受体阻断剂而显著地减弱。在血量扩张时对照组与实验组血压均呈小而短暂升高,无显著差别。上述结果表明血量扩张引起的ＲＳＮＡ抑制,部分是通过迷走传入神经触发ＰＶＮ－脊髓径路介导的。     

大鼠脑胆碱能系统对血量扩张引起利尿与尿钠排泄的作用

本工作在清醒大鼠侧脑室注射胆碱能药物,观察脑胆碱能系统对血量扩张引起利尿与尿钠排泄的作用。侧脑室注射人工脑脊液后进行血量扩张引起尿流量、排钠量和排钾量显著增加(P<0.01)。侧脑室注射胆碱能 M 受体阻断剂阿托品后,血量扩张引起尿流量、排钠量和排钾量增加的效应比注射人工脑脊液组的均显著减弱(P<0.01);而侧脑室注射胆碱能 N 受体阻断剂六烃季胺后,血量扩张引起尿流量、排钠量和排钾量增加的效应与注射人工脑脊液组的相比无显著差异(P>0.05)。侧脑室注射人工脑脊液或阿托品大鼠的肾小球滤过率(GFR)与肾血浆流量(RPF)在血量扩张后均无显著变化(P>0.05)。上述结果表明:大鼠脑胆碱能M 受体参与血量扩张引起利尿与尿钠排泄反应的调节。脑 M 受体的这种作用不是通过改变GFR 和 RPF,而可能是通过未明神经液递机制直接影响肾小管对水钠的重吸收。     

肾多巴胺受体对血量扩张和脑室高张盐溶液注射引起促钠排泄的作用

本工作观察麻醉兔用氟哌啶醇阻断肾多巴胺受体对血量扩张（ＶＥ）和脑室高张盐溶液注射（ＩＣＨＮａ）引起促钠排泄反应的影响。在ＶＥ实验中。对照组与氟哌啶醇组排销量增加峰值分别为６５．６±１５．０与１９．０±５．５μｍｏｌ／ｍｉｎ（Ｐ＜０．０２）;在ＩＣＨＮａ实验中,对照组与氟哌啶醇组排钠量增加峰值分别为２８．９±４．６与２９．０±５．８μｍｏｌ／ｍｉｎ（Ｐ＞０．０５）,在肾多巴胺受体完好兔实验中,ＶＥ＋ＩＣＨＮａｇ;起的促钠排泄大于ＶＥ（Ｐ＜０．０１）或ＩＣＨＮａ（Ｐ＜０．０１）引起的反应。肾多巴胺受体阻断也可显著减弱ＶＥ＋ＩＣＨＮａ引起促钠排泄反应。结果表明：肾多巴胺受体阻断显著减弱ＶＥ以及ＶＥ＋ＩＣＨＮａ引起促钠排泄,对ＩＣＨＮａ的反应无效;在正常兔ＶＥ＋ＩＣＨＮａ引起促钠排泄显著大于各单一刺激的反应。     

AT1受体在脑内胆碱能刺激引起的钠水排泄反应中的作用

目的和方法 :本工作通过整体实验和免疫组化的方法 ,观察脑血管紧张素能AT1受体在侧脑室注射氨甲酰胆碱引起的促钠排泄反应中的作用和下丘脑室旁核TH IR的变化。结果 :用脑血管紧张素能AT1受体阻断剂Losar tan( 2 0 μg)预处理 ,可部分阻断侧脑室注射氨甲酰胆碱引起的促钠排泄反应和利尿作用 (P <0 .0 5)。免疫组化实验显示侧脑室给予氨甲酰胆碱后 40min ,下丘脑室旁核 (PVH)、室周核 (Pe)、弓状核 (Arc)和下丘脑前区后部 (AHP)的酪氨酸羟化酶 (TH )免疫反应活性明显增强。Losartan预处理后侧脑室再注射氨甲酰胆碱 ,除PaPo的免疫反应活性未发生明显变化外 ,上述其余神经核团的TH免疫反应活性明显下降。结论 :在脑胆碱能刺激引起的钠水排泄反应中有AT1受体的参与 ;阻断脑血管紧张素能AT1受体对胆碱能刺激引起Arc、Pe和AHP的儿茶酚胺能神经元兴奋性有下调作用。提示脑血管紧张素能和儿茶酚胺能神经通路在下丘脑室旁核等脑区共同参与介导了脑内胆碱能刺激引起的促钠排泄反应 ,同时血管紧张素能神经元还影响儿茶酚胺能神经元的功能活动     

兔下丘脑室旁核刺激引起的肾交感神经传出活动的抑制

本实验用家兔,氯醛糖及尿酯混合静脉麻醉,制动,人工呼吸,颈部分离出三对神经——迷走、窦及主动脉神经,以备实验中切断。记录股动脉压、肾交感神经传出性放电活动(RSED)及其频率幅度直方图。借助脑立体定向仪刺激下丘脑室旁核,当刺激较强时,在交感神经放电短暂增加之后,可引起血压升高及RSED抑制。这一抑制过程可分为两个时相:血压不变期间的初期抑制时相及与血压升高同时并存的后期抑制时相。实验发现RSED总抑制时程及后期抑制时程均与血压变动具有正相关关系,而初期抑制时程与血压变动无相关关系。切断压力感受性神经前后,虽初期抑制时程的均值无显著差异,但在切断压力感受性神经后,总抑制时程及后期抑制时程的均值大大缩短。当用较弱刺激施于室旁核时,可不引起血压变化,但仍能引起RSED抑制。这个抑制亦可因切断压力感受神经而显著缩短。上述实验结果表明:(1) 在中枢内存在着一个室旁核-肾交感传出系统的抑制机制;(2) 初期抑制来源于中枢性抑制机制,而后期抑制时相主要来源于压力感受性反射,但亦有中枢抑制机制的参与;(3) RSED的中枢抑制可能并不是兴奋后压抑,而是自室旁核至脊髓交感节前神经元的主动性抑制。     

Role of the paraventricular nucleus in renal excretory responses to acute volume expansion: role of nitric oxide

Acute volume expansion (VE) produces a suppression of renal sympathetic nerve discharge (RSND) resulting in diuresis and natriuresis. Recently, we have demonstrated that the endogenous nitric oxide (NO) system within the paraventricular nucleus (PVN) produces a decrease in RSND. We hypothesized that endogenous NO in the PVN is involved in the suppression of RSND leading to diuretic and natriuretic responses to acute VE. To test this hypothesis, we first measured the VE-induced increase in renal sodium excretion and urine flow with and without blockade of NO, with microinjection of NG-monomethyl-L-arginine (L-NMMA; 200 pmol in 200 nl), within the PVN of Inactin-anesthetized male Sprague-Dawley rats. Acute VE produced significant increases in urine flow and sodium excretion, which were diminished in rats treated with L-NMMA within the PVN. This effect of NO blockade within the PVN on VE-induced diuresis and natriuresis was abolished by renal denervation. Consistent with these data, acute VE induced a decrease in RSND (52% of the baseline level), which was significantly blunted by prior administration of L-NMMA into the PVN (28% of the baseline level) induced by a comparable level of acute VE. Using the push-pull perfusion technique, we found that acute VE induced a significant increase in NOx concentration in the perfusate from the PVN region. Taken together, these results suggest that acute VE induces an increase in NO production within the PVN that leads to renal sympathoinhibition, resulting in diuresis and natriuresis. We conclude that NO within the PVN plays an important role in regulation of sodium and water excretions in the volume reflex via modulating renal sympathetic outflow.     

Changes induced by 6-hydroxydopamine in the paraventricular nucleus

Summary Remodelling of catecholaminergic (CA) fibers after cerebral intraventricular 6-hydroxydopamine (6-OH-DA) administration was evaluated quantitatively in the paraventricular nucleus (PAR) of young adult rats, using fluorescence microscopy (FM) and electron microscopy (EM). Fluorescent CA varicosities and CA boutons (marked with 5-OH-DA) were counted after survival periods of 4, 21, 56 or 180 days. Four days after 6-OH-DA treatment, the number of fluorescent varicosities dropped to 45% of control numbers but was restored to 79% of control values by 180 days. In the EM study, marked boutons had dropped more dramatically: to 12% of control numbers, after 4 days and 54% by 180 days post-neurotoxin. These data provide strong evidence that substantial but incomplete restoration of CA terminals occurred in PAR. It is of interest that, in all survival intervals, percentage reductions in numbers of CA terminals were more extreme when EM was used for quantification. Nevertheless, the trends indicating partial restoration of terminal numbers with time were parallel in the FM and EM studies. Structures identified as CA growth cones in PAR contained a feltwork of fine filaments together with mitochondria, granular vesicles (often with electron-dense cores marked by the 5-OH-DA label), vacuoles and smooth-surfaced reticulum. The presence of growth cones, some of which persisted 11 months after neurotoxin administration, further supports the inference that a regenerative response of CA elements was evoked in PAR by the 6-OH-DA treatment.Presented in part at IV International Catecholamine Symposium in California, September 1978     

室旁核在刺激中脑防御反应区诱发防御性升压反应中的作用

雄性ＳＤ大鼠,用乌拉坦（７００ｍｇ／ｋｇ）和氯醛糖（３０ｍｇ／ｋｇ）腹腔麻醉。实验结果：（１）每隔５ｍｉｎ电刺激中脑导水管周围灰质背侧部“防御反应区”（ｄＰＡＧ）,持续观察５０ｍｉｎ,可见恒定的升压反应。若电解毁单侧室旁核（ＰＶＮ）区。１ｈ后,电刺激中脑ｄＰＡＧ区诱发的升压反应幅度部分减小。而损毁穹隆部、下丘脑前部、下丘脑背内侧核、下丘脑腹内侧核则无上述效应。（２）电刺激或微量注射高半胱胺酸（ＤＬ     

下丘脑室旁核的心血管调节功能研究进展

下丘脑室旁核 (PVN)是自主性和内分泌性反应的重要整合中枢 ,且在维持心血管活动的动态平衡中起着关键作用。本文简要归纳了PVN的形态结构、纤维联系 ,并详细叙述其对心血管活动的调节及与心血管疾病的关系。