肾动脉内注射L-精氨酸抑制肾神经传入纤维的自发活动

研究旨在应用记录肾传人神经多单位和单位放电的方法,观察肾动脉内注射L—精氨酸对麻醉家兔肾神经传人纤维自发放电活动的影响。结果表明：(1）肾动脉内注射L—精氨酸(0．05、0．24和0．48mmol/kg)可呈剂量依赖性地抑制肾传人纤维的活动,而动脉血压不变;(2)静脉内预先注射一氧化氮合酶抑制剂L—NAME(0．11mmol/kg),可完全阻断L—精氨酸对肾传人纤维的抑制;(3)肾动脉注射一氧化氮(N0)供体SIN—1(3．75μmol/kg)也可抑制肾传入神经的活动。以上结果提示：肾动脉内应用N0前体L—精氨酸和N0供体SIN—1均可抑制肾传入纤维的自发活动。     

肾动脉内注射辣椒素兴奋肾神经传入纤维的自发活动

应用记录肾传入神经多单位和单位放电的方法,观察肾动脉内注射辣椒素对麻醉家兔肾神经传入纤维自发放电活动的影响。结果表明：(1)肾动脉内注射辣椒素20、40和60nmol／kg可呈剂量依赖性地兴奋肾传入纤维的活动,而动脉血压不变;(2)静脉内预先应用辣椒素受体阻断剂钌红(40mmol／kg),可完全阻断辣椒素对肾传人纤维的兴奋作用。(3)静脉内预先注射一氧化氮合酶抑制剂L-NAME(0．1mmol／kg),能延长并增强肾传入神经对辣椒素的反应。以上结果提示：肾动脉内应用辣椒素可兴奋肾传人纤维的自发放电活动。一氧化氮作为抑制因素参与辣椒素诱导的肾传入神经兴奋。     

电刺激肾神经传入纤维对肾水钠钾排出的影响

本文探讨肾神经传入纤维对肾排泄功能的影响及其机制。在戊巴比妥钠麻醉猫中,切除双侧颈动脉窦神经、主动脉神经和迷走神经(SAD+VD),电刺激肾神经传入纤维使动脉血压明显升高,去神经肾的尿量,排钠量显著增多,排钾量和肾小球滤过率不变。神经完好肾的排钠量显著增加,尿量、排钾量和肾小球滤过率均无显著变化。在刺激肾神经传入纤维时,将动脉血压控制在对照期血压水平,两侧肾的尿量、排钠量、排钾量显著减少;神经完好肾的肾小球滤过率减少,而去神经肾的肾小球滤过率无显著改变。脊髓横断不能消除神经完好肾上述肾排泄功能的改变,但可消除去神经肾排泄功能的改变。这些结果表明,在SAD+VD猫中,控制动脉血压不变时,刺激肾神经传入纤维可使有神经肾和去神经肾排尿、排钠和排钾减少。在神经完好肾中这些反应可在脊髓水平完成。     

心室内注射腺苷对肾交感神经传出活动的影响

在切断两侧缓冲神经和迷走神经的麻醉大鼠,观察心室内注射腺苷及其同系物对肾交感神经传出活动的影响。心室内冲击注射腺昔（0．5μmol／kg,0．1ml）时,肾交感神经传出放电（RSNA）增加41．9±6．08％（P＜0．001）,并引起平均动脉血压（MAP）先短暂升高1．39±0．19kPS（P＜0．001）和随后下降3．74±0．64kPa（P＜0．001）,以及心率（HR）减慢95±14bpm（P＜0．001）。为了确定何种受体亚型介导腺苷所致RSNA增加,又分别应用了选择性腺昔A1受体激动剂[（-）-N6－（2－Phenylisopropyl）adenosine,R－PIA]和A2受体激动剂[5＇－（N－ethylcarboxamido）adenosine,NECA]。无论R－PIA（0．05μmol／kg,0．1ml）或NECA（0．05μmol／kg,0．1ml）均使MAP下降和HR减慢,且作用持续时间较腺苷的明显延长;R－PIA使RSNA增加31．6±5．21％（P＜0．001）,但NECA对RSNA无明显影响。选择性腺苷A1受体拮抗剂（8－cyclopentyl－1,3－dipropylxanthine,DPCPX）可完全抑制腺苷对RSNA的兴奋效应。切除双侧星状神经节后,腺苷兴奋RSNA的效应消失。以上结果提示,腺苷可通过A1受体激活心交感神经传入纤维,反射地增强肾交感神经的传出活动。     

肾动脉内注射内皮素—1对麻醉大鼠肾神经传入放电的影响

本实验旨在观察肾动脉内注射ＥＴ－１对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）和肾神经传入放电（ＡＲＮＡ）的影响,以及ＥＴＡ受体阻断剂ＢＱ－１２３和硝苯吡啶（Ｎｉｆ）对ＥＴ生物学效应的拮抗作用。结果如下：（１）肾动脉注射ＥＴ－１（１μｇ／ｋｇ）后,平均动脉压（ＭＡＰ）先有短暂的降低（由１３．７７±０．１３ｋＰａ降至１０．２±１．１２ｋＰａ）,随后为较显著的持久增高,增值达３．４４±１．６０ｋＰａＰ＜０．００１）,ＨＲ无明显变化,ＡＲＮＡ增加１０８．３３±１６．６７％（Ｐ＜０．００１）。（２）肾动脉内注射ＥＴＡ受体选择性拮抗剂ＢＱ－１２３（１５０μｇ／ｋｇ）,ＥＴ－１的上述效应即被拮抗。与ＥＴ组相比差异非常显著（Ｐ＜０．００１）。（３）肾动脉内注射二氢吡啶敏感性Ｌ－型钙通道阻断剂Ｎｉｆ（０．１ｍｇ／ｋｇ）,也可明显抑制ＥＴ－１的上述效应,与ＥＴ组相比差异十分显著（Ｐ＜０．００１）。以上结果表明：肾动脉内注射ＥＴ－１引起的麻醉大鼠ＭＡＰ增高和ＡＲＮＡ积分增加的作用,可能是由ＥＴＡ受体介导的,其作用的细胞机制可能在于胞内钙超载     

肾神经传入纤维在DOCA—salt大鼠高血压形成中的作用

于大鼠皮下埋入含醋酸去氧皮质酮（ＤＯＣＡ）的交管以形成ＤＯＣＡ－ｓａｌｔ高血压,其中一组动物在埋管前切除（Ｔ９－Ｌ２）脊髓右侧背根神经,每周以尾套法测定大鼠收缩压,埋管后６周测定大鼠脑和血浆中儿茶酚胺（ＣＡ）和血管紧张素Ⅱ（ＡｎｇⅡ）的浓度,用电脑血管显微图像分析系统测量血管的结构变化。与对照鼠相比,ＤＯＣＡ－ｓａｌｔ高血压大鼠下丘脑和延脑 肾上腺素含量和ＡｎｇⅡ放免活性及血浆去甲肾上腺素（ＮＥ）     

室旁核在刺激肾神经传入纤维对血浆皮质醇浓度影响中的作用

本文在氯醛糖麻醉猫中探讨室旁核毁损前、后,电刺激肾神经传入纤维对血浆皮质醇浓度的影响。在动脉压力感受器完整猫中,刺激肾神经传入纤维对血浆皮质醇浓度无明显影响,但在动脉压力感受器去神经和迷走神经切断(SAD+VD)后,电刺激肾神经中枢端引起血浆皮质醇浓度升高。微量注射红藻氨酸毁损双侧室旁核后,可阻断刺激肾神经传入纤维引起的血浆皮质醇浓度升高,这些结果表明:动脉压力感受性反射可抑制刺激猫肾神经传入纤维引起的血浆皮质醇浓度升高;室旁核在刺激肾神经传入纤维引起的血浆皮质醇浓度升高效应中起重要作用。     

兔小脑延髓池注射纳洛酮对刺激肾神经传入纤维血压效应的影响

本文目的在于用小脑延髓池注射(Ict)受体阻断剂的方法,观察低位脑干阿片样受体与α肾上腺素受体对刺激肾神经传入纤维和主动脉神经降压效应的影响。实验在戊巴比妥钠麻醉兔中进行。Ict人工脑脊液(CSF)对刺激肾神经传入纤维和主动脉神经的降压反应均无明显影响。Ict 550nmol纳洛酮可显著抑制刺激肾神经传入纤维的降压效应,但能明显增强刺激主动脉神经的降压效应。Ict酚妥拉明可显著抑制刺激肾神经传入纤维和主动脉神经的降压效应。Ict纳洛酮可逆转酚妥拉明对刺激主动脉神经的降压效应的抑制,但不影响酚妥拉明对刺激肾神经传入纤维的降压效应的抑制。Ict纳洛酮和酚妥拉明都不影响刺激肾神经传入纤维降压反应与主动脉压力感受性反射的抑制性相互作用。Ict酚妥拉明使MAP显著下降;纳洛酮不影响MAP,但可逆转酚妥拉明降低MAP的作用。上述结果提示,激动低位脑干的阿片样受体可增强刺激肾神经传入纤维的降压作用,减弱刺激主动脉神经的降压作用,激动α肾上腺素受体可增强刺激肾神经传入纤维和主动脉神经的降压反应     

室旁核在剌激猫肾神经传入纤维引起的血压效应中的应用

The purpose of this study is to investigate the role of paraventricular nucleus of the hypothalamus (PVN) and alpha 1 adrenergic receptor of PVN in the pressor responses to stimulation of renal afferent nerve in alpha 1-chloralose-anesthetized cats with carotid sinoaortic denervation and vagotomy. The pressor response to stimulation of renal afferent nerve consisted of a primary and a second components. The primary component response was completely blocked while the second component was not blocked by autonomic blocking agents (hexomethonium and atropine). Bilateral lesions of PVN greatly attenuated the pressor response before and after autonomic blockade. Intracerebroventricular and PVN injection alpha 1, adrenergic antagonist (prazosin) significantly decreased in the pressor response to stimulation of renal afferent nerve. These results indicate that paraventricular nucleus of the hypothalamus and alpha 1 adrenergic receptors in central nervous system, especially in PVN, play an important role in the pressor responses to stimulation of renal afferent nerve.     

NO和ANP对内皮素引起大鼠肾神经传入放电增加的阻抑作用

目的和方法：采用电生理学技术观察一氧化氮（NO）和心房钠尿肽（ANP）对肾动脉内注射内皮素（ET）所致麻醉大鼠肾神经传入放电（RANA）的影响。结果：①肾动脉内注射ET－1后平均动脉压（MAP）先有短暂的降低随后为较显著的持久增高,RANA明显增加;②肾动脉内分别注射NO前体L－Arg和ANP后,ET－1的上述效应即被阻抑。结论：肾动脉ET－1引起RANA明显增加,百此效应可被同一途径注射NO和ANP所消除。     

最后区注射腺苷对大鼠血压、心率和肾交感神经放电的影响

在 5 3只麻醉Sprague Dawley大鼠观察了最后区内微量注射腺苷 (1ng/ 6 0nl)对平均动脉压 (MAP)、心率(HR)和肾交感神经放电 (RSNA)的影响。实验结果如下 :(1)最后区内微量注射Ado后 ,MAP、HR和RSNA分别由13 76± 0 46kPa、35 6 2 8± 4 2 5bpm和 10 0± 0 %下降至 11 2 3± 0 49kPa (P <0 0 0 1)、336 91± 5 2 3bpm (P <0 0 1)和70 95± 5 19% (P <0 0 0 1) ;(2 )静脉注射非选择性腺苷受体拮抗剂 8 苯茶碱 (8 phenyltheophylline,15 0 μg/kg ,0 2ml)和选择性腺苷A1受体拮抗剂 (8 cyclopentyl 1,3 dipropylxanthine,5 0 0 μg /kg ,0 2ml)后 ,腺苷的上述抑制效应可被完全阻断 ;(3)静脉注射ATP敏感性钾通道阻断剂格列苯脲 (5mg/kg ,0 2ml)后 ,腺苷的上述效应也被消除。以上结果提示 ,最后区微量注射腺苷对血压、心率和肾交感神经放电有抑制作用 ,此作用与A1受体介导的ATP敏感性钾通道开放有关。     

腺苷易化大鼠颈动脉窦压力感受器的活动

在36只麻醉大鼠,以隔离灌流颈动脉窦区记录窦神经传入放电的方法观察了腺苷（adenosine,Ado）对颈动脉窦压力感受器传入放电的影响。所得结果如下：（1）以75μmol／LAdo隔离灌流大鼠左侧颈动脉窦区时,窦内压-窦神经传入放电积分（ISP－ISNA）关系曲线向左上方移位,曲线最大斜率（PS）由（18．75±0．12）％／kPa增至（22．21±0．11）％／kPa（P＜0．001）,最大积分值（PIV）由（209．83±2．57）％增至（239．17±1．75）％;阈压（TP）和饱和压（SP）则分别从（8．57±0．24）和（22．99±0．34）下降至（7．15±0．23）kPa（P＜0．001）和（21．21±0,43）kPa（P＜0．01）。再分别以125和175μmol／LAdo灌流,机能曲线进一步向左上方移位,PS、TP和SP的变化均呈明显的剂量依赖性。（2）用腺苷选择性A1受体拮抗剂8－cyclopentyl－1,3－dipropylxanthine（0．134mmol／L）预处理后,Ado的上述效应即被阻断。（3）先给予KATP通道阻断剂格列苯脲（10μmol／L）亦可取消腔苷对窦神经传入放电的影响。结果表明,在体隔离灌流大鼠颈动脉窦区条件下,Ado对颈动脉窦压力感受器活动有易化作用,此作用似与腺苷A1受体介导的KATP通道开放有关。     

肾神经在肾缺血预处理对麻醉家兔心脏保护中的作用

在氨基甲酸乙酯麻醉家兔上,观察肾脏缺血预处理(RIP)对缺血-再灌注心肌的影响,旨在证实RIP对心肌有无保护效应,并明确肾神经在其中的作用。所得结果如下(1)在心脏45min缺血和180min再灌注过程中,血压、心率和心肌耗氧量呈进行性下降;心外膜电图ST段在缺血期明显抬高,再灌注过程中逐渐恢复到基础对照值。心肌梗塞范围占缺血心肌的55.80±1.25%。(2)RIP时心肌梗塞范围为36.51±2.8%,较单纯心肌缺血-再灌注显著减少(P<0.01),表明RIP对心肌有保护作用。(3)肾神经切断可取消RIP对心肌的保护效应,但肾神经切断本身对单纯缺血-再灌注所致的心肌梗死范围无明显影响。(4)肾缺血(10min)时,肾传入神经放电活动由0.14±0.08增至0.65±0.12imp/s(P<0.01)。(5)预先应用腺苷受体拮抗剂8-苯茶碱可明显减弱肾缺血所激活的肾传入神经活动,提示肾传入活动的增强是由肾缺血产生的腺苷所介导。以上结果表明,肾短暂缺血-再灌注所诱发的肾神经传入活动在RIP心肌保护效应中起重要作用。     

Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of alpha1- and alpha2-adrenoceptors on renal sensory nerve fibers

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating alpha-adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the alpha(1)- and alpha(2)-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49 degrees C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 +/- 900 and 4,870 +/- 670%.s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 +/- 210%.s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 +/- 1 to 16 +/- 1 pg/min, and PGE(2) release, from 77 +/- 11 to 161 +/- 23 pg/min, suggesting a role for PGE(2) in the norepinephrine-induced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE(2). PGE(2) enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating alpha(1)- and alpha(2)-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE(2).     

Vagal afferent activity and renal nerve release of dopamine

To investigate the involvement of vagal afferents in renal nerve release of catecholamines, we compared norepinephrine, dopamine, and epinephrine excretion from innervated and chronically denervated kidneys in the same rat. The difference between innervated and denervated kidney excretion rates was taken as a measure of neurotransmitter release from renal nerves. During saline expansion, norepinephrine excretion from the innervated kidney was not statistically greater than from denervated kidneys. Vagotomy increased norepinephrine release from renal nerves. Thus vagal afferents participated in the suppression of renal sympathetic nerve activity during saline expansion. No significant vagal control of dopamine release by renal nerves was detected under these conditions. Bilateral carotid ligation stimulated renal nerve release of both norepinephrine and dopamine in saline-expanded rats. The effects of carotid ligation and vagotomy were not additive with respect to norepinephrine release by renal nerves. However, the baroreflex-stimulated renal nerve release of dopamine was abolished by vagotomy. Electrical stimulation of the left cervical vagus with a square wave electrical pulse (0.5 ms duration, 10 V, 2 Hz) increased dopamine excretion exclusively from the innervated kidney of hydropenic rats. No significant change in norepinephrine excretion was observed during vagal stimulation. Increased dopamine excretion during vagal stimulation was associated with a larger natriuretic response from the innervated kidney than from its denervated mate (p less than 0.05). We conclude that under appropriate conditions vagal afferents stimulate renal release of dopamine and produce a neurogenically mediated natriuresis.     

电刺激大鼠腓肠神经引起Aδ、 C类传入神经纤维的背根反射

在距脊髓约 15mm处切断大鼠L5背根 ,将中枢端分成 4～ 5条细束 ,电刺激腓肠神经在背根细束上记录背根反射 (dorsalrootreflex ,DRR)。共记录到DRR 5 1例 ,根据引起DRR所兴奋的腓肠神经纤维类别和DRR在背根逆向传出的纤维类别将DRR分为 5类 :Aαβ Aαβ·DRR、Aβδ Aδ·DRR、Aβδ C·DRR、Aαβδδ C·DRR和C C·DRR。结果证明 ,电刺激外周神经激活各类纤维不但能引起A类 (包括Aδ)纤维的DRR ,而且也能引起C类纤维的DRR。记录的Aδ·DRR和C·DRR为细纤维传入终末产生突触前抑制提供了客观指标 ,为DRR逆向传出冲动到达外周组织 ,释放神经肽类递质 ,调节外周效应器的功能提供了证据     

延髓腹外侧头端区注射肾上腺髓质素对大鼠血压、心率和肾交感神经活动的影响

本研究在 3 4只麻醉Sprague Dawley大鼠观察了延髓腹外侧头端区内微量注射肾上腺髓质素 ( 10μmol/L ,2 0 0nl)对平均动脉压 (MAP)、心率 (HR)和肾交感神经放电 (RSNA)的影响。实验结果如下 :( 1)延髓腹外侧头端区内微量注射肾上腺髓质素可引起MAP、HR、和RSNA明显增加 ,分别由 99 0 9± 3 3 2mmHg ,3 70 78± 7 84bpm和 10 0± 0 %增至 113 5 7± 3 64mmHg (P <0 0 0 1) ,3 83 2 8± 7 3 8bpm (P <0 0 0 1)和 12 3 72±2 74% (P <0 0 0 1) ;( 2 )降钙素基因相关肽受体阻断剂CGRP8 3 7( 10 0 μmol/L ,2 0 0nl)不能阻断肾上腺髓质素的上述效应 ;( 3 )静脉注射NO前体L 精氨酸 ( 10 0mg/kg ,0 2ml)可消除肾上腺髓质素的上述效应。以上结果提示 ,肾上腺髓质素作用于延髓腹外侧头端区可产生显著的心血管作用 ,此作用不是由降钙素基因相关肽受体介导 ,但可被NO所阻断