采用逆转录-聚合酶链式反应检测了慢性足底电击结合噪声应激致高血压大鼠下丘脑、延髓、中脑、垂体和肾上腺等组织中编码肾上腺髓质素的肾上腺髓质素前肽原(preproadrenomedullin, ppADM) 基因以及ADM 的特异性受体组件降钙素受体样受体(calcitonin-receptor-like receptor，CRLR)和受体活性调节蛋白2和3(receptor-activity- modifying proteins, RAMP2 和RAMP3) 表达的变化。我们观察到：与对照组相比，以3- 磷酸甘油醛脱氢酶作为内参照，15d足底电击结合噪声应激引起下丘脑、垂体和肾上腺中ppADM mRNA表达上调，而在延髓和中脑表达明显下调(P<0.01 或 P<0.05); CRLR 基因表达量正常时在下丘脑相对较高，应激15 d 后CRLR 表达在延髓、中脑和下丘脑下调(P<0.01 或 P<0.05), 而在垂体和肾上腺的表达无明显变化；应激后RAMP2 基因在延髓和下丘脑表达上调，而在肾上腺表达显著下调(P ＜ 0.01), 其他部位无明显变化；RAMP3 基因在对照组大鼠的中脑和下丘脑表达较高，在应激性高血压大鼠的下丘脑和垂体表达上调(P<0.01 或P<0.05), 而在中脑和肾上腺表达下调(P<0.05), 在延髓中的表达变化无统计学差异。上述结果提示：慢性足底电击结合噪声应激引起明显的中枢和下丘脑- 垂体- 肾上腺轴ADM 及其受体组件CRLR/RAMP2 或CRLR/RAMP3 基因的表达变化。但慢性应激后中枢源性ADM 及其受体的表达变化对应激和血压的调节以及在应激致高血压中的确切作用及机制尚待进一步研究。

采用多管微电泳结合细胞外记录的方法研究了肾上腺髓质素(adrenomedullin, ADM)对大鼠延髓头端腹外侧区(rostral ventrolateral medulla, rVLM)压力反射敏感性神经元电活动的作用及其可能机制。结果显示：在29 个rVLM压力反射敏感神经元中，20个神经元在30、60 和90 nA 的电流微电泳大鼠ADM (rADM)过程中，放电频率由(10.8±2.7) spikes/s分别增加到(14.6±3.6)、(19.8±4.7)和(31.9±6.4) spikes/s(P<0.05，n=20)。微电泳rADM特异性受体阻断剂人ADM (human ADM, hADM) (22-52)可明显减小神经元放电频率的增加幅度，比正常放电频率仅增15.4％ [(11.4±2.5) sipkes/s, P<0.05, n=10]，而降钙素基因相关肽1 (CGRP1)受体阻断剂hCGRP (8-37)对rADM兴奋性神经元电活动影响较小。在另外23个神经元中，10个神经元的放电频率在10、20 和40 nA 电流微电泳神经型NOS(nNOS)抑制剂7-NiNa 过程中放电减少，由正常的(10.1±3.5)spikes/s分别减少为 (7.5±2.5)、(5.3±2.1)和(3.1±1.4) spikes/s (P<0.05, n=10)。在微电泳7-NiNa 过程中同时微电泳rADM，则rADM增加神经元放电频率的效应减弱，增加幅度为基础水平的17％ [(6.2±1.9) spikes/s]。8个神经元在10、20 和40 nA电流微电泳诱导型NOS 抑制剂(iNOS) aminoguanidine (AG)过程中放电频率由(11.5±5.1) spikes/s 增加到(17.8±5.6)、(22.5±6.3)和(29.1±6.4) spikes/s (P<0.05, n=8)，rADM 与AG 同时微电泳时，AG对rADM本身增加神经元放电的效应无明显影响。上述结果提示，rADM在rVLM可通过其特异性受体或来源于nNOS 的NO作用于压力反射敏感神经元，使其活动增强而发挥调节心血管活动的作用。

Expiratory neurones, with a decrementing firing pattern during the first phase of expiration (EDEC) and located in the rostral ventrolateral medulla, are thought to be involved in the network generating respiratory rhythm, which also includes expiratory neurones with augmenting firing patterns (E-AUG). We used crosscorrelation to detect their synaptic interconnections and connections to phrenic motoneurones in 32 vagotomised, decerebrate, paralysed and ventilated male rats. Pairs of neurones were recorded extracellularly with glass-insulated tungsten microelectrodes and the whole phrenic nerve with bipolar silver wire electrodes. Of the 79 crosscorrelograms computed between pairs of E-DEC neurones, 8 (-10%) showed evidence for inhibitory connections. Of the 67 cross-correlograms computed between EDEC and E-AUG neurones, 5 (7.5%) showed evidence for a monosynaptic inhibition of the E-AUG neurone by the E-DEC neurone, while 3 (4.5%) showed evidence for a monosynaptic inhibition of the E-DEC neurone by the EAUG neurone. An inhibitory connection from E-DEC neurones to phrenic motoneurones was detected in 5 (-2%) of the cross-correlograms, and from E-AUG neurones to phrenic motoneurones in 4 (-3.7%). These results are the first demonstration that network models of rhythm generation in the rat involving reciprocal inhibition between E-DEC and E-AUG neurones could have a neurophysiological basis, and the first to demonstrate that phrenic motoneurones are inhibited during the early phase of expiration by E-DEC neurones.

在α2氯醛糖麻醉的猫上, 结扎左心室冠状动脉前降支(LAD)一小分支, 对动物胆囊浆膜面予以缓激肽(BK), 可反射性地诱发血压、左心室内压升高、±dP/dtmax增大、心率加快,同时用超声单晶片声纳测微系统记录局部心壁运动, 发现BK可以反射性地引起LAD小分支远端所支配的心肌运动功能减弱。电针内关穴对BK诱发的升压反应有抑制作用, 并可改善局部心肌运动功能。静脉注射纳洛酮(014mg/kg) 能翻转电针效应。结果表明, 电针能够抑制BK诱发的升压反应和改善局部心肌运动功能, 该效应与内源性阿片肽有关。

The main source of expiratory drive to respiratory muscles in the rat is thought to be the caudal expiratory neurones. However, their projections to the spinal cord and the coordination of the population activity with the respiratory cycle are largely unknown. We examined their bulbospinal projections using antidromic activation, and the coordination of their activity using crosscorrelation. Of 76 expiratory neurones examined, 40% projected to the C2 segment of the spinal cord, all unilaterally and all but 4 to the contralateral side. Thirteen contralateral axons were located in the ventromedial funiculus, when activation thresholds were less than 25 μA. For 29 neurones, the mean (±SEM) conduction velocity, calculated from the single-point activation and a measure of the direct distance between recording and stimulating electrodes, was 7.4±0.4 m/s. We calculated 88 crosscorrelograms from ipsilateral pairs of expiratory neurones recorded on the same side of the medulla, and 176 contralateral pairs recorded from opposite sides of the medulla. All of the latter were featureless, but 23% of cross-correlograms for ipsilateral pairs displayed broad peaks at time zero, which we interpreted as due to activation of both neurones from a common source. We conclude that in the adult rat, approximately half of the caudal expiratory neurones project unilaterally and contralaterally to the spinal cord and, although common activation serves to coordinate some of the ipsilateral population, we suggest that neither common activation nor excitatory cross-connections exist as sufficient means for coordinating left and right populations to the same respiratory rhythm.