电刺激延髓最后区对血浆肾素活性及肾交感神经活动的影响

实验在68只家兔上进行。乌拉坦麻醉。用RM-6000型多道仪同步记录呼吸(Respir)、血压(BP)、心率(HR)及肾神经放电(RSNA)。用放免法测定血浆肾素活性(PRA)。应用外径0.3mm的双芯同心电极置于延髓最后区(AP)处进行电刺激,每30s刺激4s。实验分为三组。第一组仅刺激AP观察到PRA增加了91％,RSNA出现以兴奋为主的三种放电形式,BP升高,HR减慢,呼吸无显著变化。第二组去除双侧肾神经后再刺激AP,PRA增加甚微,RSNA及血流动力学反应与第一组刺激前后的变化相似。第三组注射心得安后,刺激AP,这时除PRA明显抑制外,RSNA、BP、HR及呼吸亦与第一、第二组刺激前后的变化相似。上述结果表明电刺激兔AP能引起肾素释放增加,肾交感神经放电及血流动力学活动增强。     

家兔延髓区域阻滞对呼吸的影响

实验在麻醉、切断迷走神经的家兔上进行。记录双侧膈神经放电和气管内压作为呼吸的指标。用尖端直径为70—100μm的玻璃微管接微量注射器,脑内注入1％普鲁卡因,双侧对称地阻滞闩前2.0—3.0mm,中线旁开2.0—2.5mm,背侧表面下3.5—4.5mm的区域后,38只兔都出现了可逆性呼吸停止。双侧性电损毁此区,则可造成不可逆性呼吸停止。以同法注入同量生理盐水,则对呼吸无影响。经组织学检查,此区范围相当于Meessen图谱的面后核内侧区——包括面后核(Nr.Ⅶ)内侧部、网状小细胞核(R·pc)腹侧部、网状巨细胞核(R·gc)背外侧部和外侧网状核(Rl)的内侧部分。用同样方法阻滞延髓头端区、孤束核区及疑核尾端区、对呼吸节律均无明显影响。用1％普鲁卡因局部麻醉延髓腹侧面的中枢化学感受器I(s)区,呼吸也无明显变化。结果提示,面后核内侧区的一些结构可能在形成呼吸节律中起重要作用。     

电刺激猫小脑顶核对动脉血压和肾交感神经放电的影响

在38只麻醉及人工呼吸的猫,观察到电刺激小脑顶核嘴侧部能引起动脉血压显著升高;肾交感神经放电于刺激期间显著增加。去缓冲神经对刺激顶核所引起的血压反应的幅度和肾交感神经放电均无明显影响,但可明显延长血压反应升高相以及血压恢复期的时间。静脉注射氯庄定引起血压降低、心率减慢及肾交感神经放电的抑制,并能减弱刺激顶核引起的血压反应,但增强了刺激顶核引起的肾神经放电的变化。电解损毁延髓腹外侧面引起血压降低及肾交感神经放电的抑制,然而无论单侧还是双侧损毁延髓腹外侧面都不能阻断刺激顶核所引起的血压和肾交感神经放电的反应。以上结果表明,电刺激顶核能引起明显的心血管反应,其反应的下行性通路可能不通过延髓腹外侧面。     

电刺激兔下丘脑视前内侧区对Oddi氏括约肌肌电的影响

下丘脑是内脏神经的较高级中枢。它对胃肠和心血管话动都具有重要的调整作用。关于下丘脑对胆道系统话动的调整作用在国内、外报道较少。近年来我们研究组分别报道了电刺激兔下丘脑前区、内侧区对胆汁流量、胆囊压力有明显的影响。本组实验是观察电刺激兔下丘脑视前内侧区(MPO)对Oddi氏括约肌肌电活动的影响,并初步分析引起这种变化的机制。     

肾神经在扩张心房时对尿量和尿钠排出的作用

单侧肾去神经的麻醉狗,用乳胶小囊扩张肺静脉-心房连接部,观察到神经完好肾的尿流量与排钠量均显著增加(P<0.01);去神经肾的尿流量仍显著增加(P<0 01),但排钠量无明显变化(P>0.05);两侧肾的肾小球滤过率(GFR)及肾血浆流量(RPF)均保持稳定;神经完好肾的静脉血浆肾素活性(PRA)及血管紧张素Ⅱ水平(PAⅡ)均明显降低,PAⅡ降低的幅度与尿流量增加的幅度无相关(r=-0.2975,P>0.05);与排钠量增加的幅度也无相关(r=-0.2359,P>0.05);去神经肾的PRA和PAⅡ都没有显著变化。说明在刺激心房感受器引起的利尿与尿钠排泄的反应中,肾神经主要促进肾对尿钠的排出。肾神经的这种作用既不是通过改变GFR和RPF,也不是抑制肾素的释放,而可能是由于直接影响肾小管对钠的重吸收。     

脑室注射高低渗NaCl溶液对血浆肾素活性及肾交感神经活动的影响

第三脑室注射高渗NaCl溶液可引起肾交感神经活动(RSNA)减弱和血浆肾素活性(PRA)降低,低渗NaCl的作用则相反,引起KSNA及PRA升高。PRA和RSNA变化呈一定的正相关,切除肾神经后高、低渗NaCl对PRA的影响减弱或消失,表明脑室内Na~ 浓度改变后主要经肾交感神经的传出通路影响肾素释放。     

大鼠下丘脑内一氧化氮合酶阳性神经元的分布

用ＮＡＤＰＨ－ｄ组织化学方法观察了大白鼠下丘脑内一氧化氮合酶（ＮＤＳ）阳性神经元的分布及形态特征。结果显示：在视上核、室旁核的大细胞部、环状核、穹窿周核、下丘脑外侧区、下丘脑腹内侧核、下丘脑背内侧核、乳头体区大部分核团均可见一氧化氮合酶阳性神经元聚集成团。在视前内侧区、视前外侧区、下丘脑前区、下丘脑背侧区、下丘脑后区、室周核、室旁核小细胞部及穹窿内可见散在的一氧化氮合酶阳性神经元。室周核内可见呈阳性反应的接触脑脊液神经元的胞体及突起。一氧化氮合酶阳性神经元大多可见突起,有的突起上可见１～２级分支,并可见膨体。下丘脑大部分区域内可见阳性神经纤维。弓状核内可见许多弧形纤维连于第三脑室室管膜和正中隆起。     

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。     

刺激家兔肾内感受器和肾传入神经的血流动力学效应

在39只麻醉家兔观察刺激肾脏机械和化学感受器以及电刺激肾传入神经的血流动力学效应。增加输尿管压8—22mmHg 及经输尿管向肾盂内逆向灌注 NaCl(1.0 mol/L)及 KCl(0.15mol/L)溶液时,引起平均动脉压(MAP)和心率(HR)下降;切断双侧缓冲神经后,MAP 降低更为显著。电刺激肾传入神经时,HR 减慢,MAP、肠系膜动脉和后肢动脉灌流压降低,左心室收缩压及其微分值下降,心输出量(CO)和总外周阻力(TPR)减小;切断双侧窦神经和减压神经后,除 HK、CO 和 TPR 外,其余各血流动力学指标的减弱更为显著。由此提示,动脉压力感受器反射对肾传入神经激活的心血管效应有缓冲作用。     

刺激蓝斑对心肌收缩力及肾交感神经放电的影响

在64只麻醉及人工呼吸的猫,观察到电刺激蓝斑(LC)能引起血压升高、心率加快,左心室收缩压升高,左心室内压最大变化率增加及肾交感神经放电(RNA)显著地增加。去缓冲神经对电刺激 LC 所引起的上述指标的增加幅度无明显影响,但可明显延长血压反应升高相以及血压恢复期的时间。LC 内微量注射谷氨酸钠可使血压下降,心率减慢,左室收缩压和左室内压最大变化率亦降低。LC 内注射海人酸,也能引起减压反应。而注射海人酸3h 后,使LC 神经元发生变性或去极化阻断时,再电刺激 LC 仍能引起明显的升压反应。以上结果表明,电刺激 LC 可使血压升高、心肌收缩力及肾交感神经放电增加,而 LC 内微量注射胞体兴奋剂则可降低血压、心率及心肌收缩力,说明电刺激 LC 引起的加压反应可能主要是兴奋了过路纤维所致,而 LC 本身神经元的兴奋引起的是减压反应。     

电刺激延髓最后区对血浆肾素活性及肾交感神经...

68 urethan-anesthetized rabbits were prepared for registration of changes of respiration, arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) due to stimulation of area postrema (AP) by rectangular pulse trains each lasting for 4 s for every 30 s. During 40 min of such a stimulation paradigm the venous blood samples were collected for radioimmunoassay of plasma renin activity (PRA) (both pre- and post-stimulation), RSNA registered and processed by a computer. Animals were divided into three groups: (1) with AP stimulation only (n = 47); (2) AP stimulation after bilateral renal denervation (n = 13); (3) AP stimulation after propranolol injection (n = 8). In Group I, a 91% increase in PRA, an augmentation of RSNA, a rise of BP and a decrease of HR were observed, while respiration did not show obvious change. In Group II, hemodynamic and RSNA response was similar to that in Group I, but PRA was not changed significantly. In Group III, the effects on BP, HR, respiration and RSNA showed no remarkable changes compared with Group I, but significant inhibition of the response of PRA [from 0.65 +/- 0.07 ng/(ml.h-1) to 0.72 +/- 0.10 ng/(ml.h-1), P > 0.05] was observed. The results mentioned above suggested that electrical stimulation of AP may induce an increase in renin release and renal sympathetic nerve activity and hemodynamic changes in rabbits.     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

肾脏和肾神经在应激、钠盐所致高血压中的作用

本工作采用电生理、生化、放免、电镜等方法,探讨了慢性应激和盐致高血压大鼠交感神经系统和肾脏功能的改变。实验在雄性ＳＤ大鼠上进行。结果表明：（１）高盐大鼠肾血浆流量（ＲＰＦ）和尿钠排泄明显增加,而应激大鼠ＲＰＦ显著下降。（２）电镜显示高盐大鼠近曲和远曲小管上皮细胞及线粒体变大,应激则使细胞萎缩、线粒体变小。（３）高盐大鼠肾皮质ＮａＫＡＴＰ酶活性下降,应激可使其恢复。（４）频谱分析显示应激大鼠低频波动（０２～０９Ｈｚ）明显增加。（５）应激导致大鼠肾素活性（ＰＲＡ）及血管紧张素Ⅱ（ＡＮＧⅡ）水平升高,并能使高盐大鼠低ＰＲＡ和ＡＮＧⅡ水平升高。（６）大鼠去除双侧肾神经后,应激无法造成血压升高、ＲＰＦ下降和ＰＲＡ、ＡＮＧⅡ上升。上述结果提示：肾交感神经系统兴奋性增加介导的肾脏机制,可能在应激和／或盐致高血压发病过程中具有重要作用。     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A₁ infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA₁ infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA₁ infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA₁ infusion. PGA₁ caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

安定降低家兔血压和减少刺激下丘脑诱发室性期前收缩的机制分析

家兔62只,用乌拉坦(700mg/kg)和氯醛醣(35mg/kg)静脉麻醉,三碘季铵酚制动,在人工呼吸下进行实验。用电刺激下丘脑近中线区的方法诱发室性期前收缩(HVE)。静脉注射安定(0.5mg/kg)可降低基础血压(BP),减弱刺激下丘脑引起升压反应(指收缩压峰值SBP_(max))和减少HVE。在双侧延髓腹外侧头端区(rVLM)微量注射氟安定(200μg溶于0.5μl中),γ-氨基丁酸(GABA)(6μg溶于0.5μl中)均能降低BP、SBP_(max)和减少HVE,若微量注射印防己毒素(7.5μg溶于0.5μl中)则可使BP上升并增多HVE。而于双侧延髓腹外侧尾端区(cVLM)微量注射同样剂量氟安定、GABA则无上述反应。安定降低BP、SBP_(max)和减少HVE的作用可被双侧rVLM区微量注射GABA受体拮抗剂荷包牡丹碱(3μg溶于0.5μl中)或印防己毒素所消除,但在双侧rVLM区微量注射甘氨酸受体拮抗剂士的宁(1μg溶于0.5μl中)、阿片受体拮抗剂纳洛酮(0.5μg溶于0.5μl中)、胆碱能阻断药阿托品(0.25μg溶于0.5μl中)、东莨菪碱(1.5μg溶于0.5μl中)后仍然存在。 上述结果提示,在双侧rVLM应用GABA受体拮抗剂可消除安定降低BP、SBP_(max)和减少HVE的作用,安定降低BP、SBP_(max)和减少HVE的作用可能通过GABA这一中间环节,而胆碱能受体、阿片受体、甘氨酸受体可能不起重要作用。     

Effects of angiotensin I-converting enzyme inhibitor, SQ 14225, in nomal men.

Effects of an orally active angiotensin I-converting enzyme inhibitor, SQ 14225, on the actions of angiotensin I (AI) infused intravenously for 120 to 390 min were studied in 5 normal men. When 20 ng/kg/min of AI infusion was started immediately after a single oral administration of 100 mg of SQ 14225, a significant rise in blood pressure (BP) was observed for the first 15 min, but BP began to fall from 17 min and returned to the pretreatment level at 45 min. This BP level continued at least to 120 min and in one subject to 180 min. In this subject BP began to rise again from 185 min and reached the level of 15 min at 390 min. Plasma AI level increased gradually from 45 min. At 15 min plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased, but then PRA began to increase and PA began to decrease. At 120 min the values of PRA and PA were similar to the pretreatment values. In one subject plasma AI and PRA began to decrease and PA began to increase after 120 or 180 min. On the other hand, in the 5 men sole AI infusion caused a continued BP rise, PRA decrease and PA increase, and sole SQ 14225 administration caused increases in plasma AI and PRA and a decrease in PA but no BP change. From these results it was concluded that complete blockade and partial inhibition of AI conversion by 100 mg of oral SQ 14225 lasted for about 2.5 and 6.5 hr, respectively and that BP rise, PRA suppression and aldosterone stimulation after AI infusion were entirely due to the actions of angiotensin II converted from AI.     

Effect of renal denervation on plasma renin activity after aortic baroreceptor deafferentation.

Renal nerves are thought to play an important role in cardiovascular regulation under both normotensive and hypertensive conditions. In the present study the effect of renal denervation on the changes in plasma renin activity (PRA) after aortic baroreceptor deafferentation (tADN) were investigated in the rat. Bilateral renal denervation did not alter arterial pressure (AP, 100 +/- 4 mmHg; 1 mmHg = 133.32 Pa), heart rate (HR, 363 +/- 12 bpm), or PRA (2.9 +/- 0.6 ng.mL-1.h-1) compared with the respective sham renal denervation values of 106 +/- 3 mmHg (AP), 385 +/- 13 bpm (HR), and 3.3 +/- 0.7 ng.mL-1.h-1 (PRA). On the other hand, bilateral tADN resulted in significant increases in AP, HR, and PRA. One and 3 days after tADN, AP was 130 +/- 4 and 127 +/- 6 mmHg, HR was 461 +/- 15 and 463 +/- 20 bpm, and PRA was 9.1 +/- 3.0 and 11.9 +/- 4.5 ng.mL-1.h-1, respectively. Renal denervation before tADN prevented the increases in AP and PRA, but it did not affect the increase in HR. These data indicate that renal denervation does not alter basal PRA in normotensive animals but prevents the increased renin release observed in neurogenic hypertension. These data suggest that the increased PRA may be one of several factors that contributes to the elevated AP after tADN.     

Plasma active renin concentration in children

In normal children aged one month to 16 years, the plasma active renin concentration (PARC) was measured with a renin immunoradiometricassay (IRMA) kit, and was compared with plasma renin activity (PRA). The IRMA for renin was found to be independent of the amount of renin substrate and not affected by the dilution of plasma samples, and was therefore proved to be a simple and reliable method. PRA measured in non-diluted plasma samples correlated well with PARC. In the age-related change, PARC in infants was significantly higher than that in older children. In infants, PARC was markedly higher in the crying state than that in the non-crying state. In normal children aged 7 to 11 years, PARC was significantly increased in the upright position compared to the supine position. These findings suggest that a hyperresponse of PARC to acute stress during blood sampling may cause an increase in active renin secretion in infants, and that stimulation by short-term standing may accelerate the activation of inactive renin or the release of active renin.     

Adrenal and vascular renin-like activity in chronic 'two-kidney, one-clip' hypertensive rats

In order to study the vascular and adrenal renin angiotensin system in the chronic phase (4 months after clipping) of 'two-kidney, one-clip' hypertension in rats, systolic blood pressure, plasma renin activity, and tissue renin-like activity in both aorta and adrenal have been measured. Renin activity in adrenal gland was studied in both the zona glomerulosa (GLO) and the remainder of the gland. Results showed an increase in vascular renin activity in chronic hypertensive rats. Moreover it was found that GLO of hypertensive rats presented a significant increase in renin-like activity compared with controls (349.43 +/- 43.86 versus 167 +/- 34.25 ng AI/g/20 h, p less than 0.01) and the fasciculata-reticular-medullar (FRM) portion also showed greater renin activity (345.16 +/- 64.36 versus 57.90 +/- 4.83 ng AI/g/20 h, p less than 0.01). The higher levels of vascular and FRM renin-like activity in chronic renal hypertension are probably a consequence of plasma renin increase. This hypothesis is supported by the fact that bilateral nephrectomy in normal rats induces a significant decrease in plasma renin activity and both aortic and FRM renin-like activity. On the other hand the GLO renin-like activity could depend on both plasma renin and local synthesis since bilateral nephrectomy induces an increase in the renin-like activity in this tissue. These data support the idea that aortic and FRM renin are, at least in part, due to plasma renin uptake and GLO renin is an autonomic system.