猫延髓头侧腹外侧区注射内皮素-1对猫心血管活动的影响

研究内皮素－１（ＥＴ－１）在猫延髓头侧腹外侧区（ｒＶＬＭ）对心血管活动的影响．方法：采用脑立体定向和脑内微量注射技术．结果：ｒＶＬＭ内微量注射 ＥＴ－１（４μｍｏｌ·Ｌ－１, ０．５μＬ）后,平均动脉压（ＭＡＰ）升高（３．７±１．３）ｋＰａ,心率增加（２９±７）ｂｅａｔｓ·ｍｉｎ－１,肾神经活动增加 ４５％±１０％,量－效呈正相关．双颈部迷走神经切断后不影响上述结果．静脉预先给予酚妥拉明 ５ ｍｇ·ｋｇ－１能显著抑制ＥＴ－１的升压作用．血浆精氨酸升压素（Ａｒｇ）含量由（１２．４± ６． ５） ｎｇ· Ｌ－１增加到（７０．３± ２４． ２）ｎｇ·Ｌ－１,并与ＭＡＰ变化显著相关,使缺血心脏心律紊乱（ＨＲｈＤ）,ＨＲｈＤ出现在结扎后（４．８±２．９）ｍｉｎ,评分为 ４．４±１．６,与对照组差异显著．结论：ｒＶＬＭ内注射ＥＴ－１影响了心血管和交感神经活动的中枢调节。     

猫头端延髓腹外侧区微量注射内皮素—1对其血压和心率的影响

为了探讨内皮素-1在头端延髓腹外侧区(the rostral ventrolateral medulla, rVLM)对心血管活动的影响。我们使用立体定位技术和微量注射的方法,用15只猫,观察了内皮素-1在该处对动脉血压(AP)、心率(HR)的影响。结果发现,随着内皮素-1剂量的增加,AP和HR也明显地升高和加快。     

猫延髓腹外侧区注射内皮素-1对其肾神经放电活动的影响

目的：探讨内皮素-1在头端延髓腹外侧区(the rostral ventrolateral medulla,rVLM)对心血管活动及肾交感神经活动的影响。方法：采用脑立体定向技术和微量注射的方法，用15只猫，观察了内皮素-1在该处对肾神经放电活动的影响。结果：随着药物剂量的增加,肾神经放电活动也增强。结论：Rvlm内的ET-1参与了交感神经活动的中枢性调节,其效果随含量的变化而改变。     

猫下丘脑视上核注射内皮素对其血压和心率的影响

猫在氯醛糖和乌拉坦混合麻醉状态下，在其下丘脑视上核注射内皮素（４ｐｍｏｌ，８ｐｍｏｌ），结果发现，大剂量内皮素（８ｐｍｏｌ）可使猫动脉血压升高；心率加快。结果提示：内皮素不仅在外周具有强列的缩血管升高血压作用，而且在中枢神经系统内，也可能做为一种神经递质调节心血管活动。     

延髓腹外侧头端注射莫索尼定对大鼠血压,心率和肾交感神经放电…

目的：观察延髓腹外侧头端（ＲＶＬＭ）注射莫索尼定（Ｍｏｘ）对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）及肾交感神经放电（ＲＳＮＡ）的影响。方法：麻醉大鼠ＲＶＬＭ注射１μＬ Ｍｏｘ１，１０，１００μｍｏｌ·Ｌ＾－１，同步记录ＢＰ，ＨＲ及ＲＳＮＡ。结果：Ｍｏｘ１，１０，１００μｍｏｌ·Ｌ＾－１分别使ＢＰ从１３．９±１．０ｋＰａ降至１３．０±１．７ｋＰａ（Ｐ〈０．０５），１３．８±１．８ｋＰａ至１１．４±１．５     

下丘脑腹内侧区注射内皮素对猫心血管系统活动的影响

为探讨内皮素对心血管中枢活动的影响，我们观察了猫下丘脑腹内侧区注射内皮素对心血管功能活动的影响．结果发现，实验条件下内皮素对正常血压，左心室压，心率等指标并无明显影响．它可能反映内皮素受体分布及其功能的差异．     

孤束核微注射内皮素-1(1-31)对心血管活动的影响

目的:观察内皮素-1(1-31)[ET-1(1-31)]在大鼠孤束核(Nucleus tracts solitarius,NTS)产生的心血管效应,并探讨其作用机制.方法:雄性SD大鼠90只,其中50只随机分为双侧NTS注射组、单侧NTS注射组和人工脑脊液(aCSF)组,分别在双侧或单侧NTS微量注射ET-1 (1-31) (0.5～2.0 pmoL)或 aCSF(100 nL),观察ET-1(1-31)在NTS内的心血管效应.11只大鼠观察ET-1(1-31) (1.0 pmoL)在NTS水平对动脉压力反射功能(BRS)产生的影响.其余29只大鼠分别预先给予ETA受体拮抗剂BQ123、ETB受体拮抗剂BQ788、非选择性谷氨酸受体拮抗剂犬尿烯酸(KYN)或对照(aCSF),探讨ET-1(1-31)在大鼠NTS内产生的心血管效应机制.结果:在大鼠NTS双侧或单侧微量注射ET-1(1-31)剂量依赖性降低大鼠血压并减缓心率;NTS双侧微注射ET-1(1-31)(1 pmoL)显著减弱大鼠BRS(P＜0.05);ETA受体拮抗剂BQ123或KYN显著减弱单侧NTS微量注射ET-1(1-31) (1.0 pmoL)产生的降低血压和减缓心率作用(P＜0.05);单侧NTS注射ETB受体拮抗剂BQ788对NTS微量注射ET-1(1-31)(1.0 pmoL)产生的降低血压和减缓心率作用没有显著的影响(P＞0.05).结论:NTS微量注射ET-1(1-31)能够降低麻醉大鼠的血压并减缓心率,其作用可能是由ETA受体和谷氨酸受体所介导.     

莫索尼定对去缓冲神经大鼠延髓腹外侧头端神经元自发电活动的影响

在去缓冲神经大鼠观察莫索尼定对延髓腹外侧头端区 (RVLM) 神经元自发电活动的影响. 向颈总动脉内注射莫索尼定2, 10, 50 μg·kg^-1后, 同步记录神经元放电图,血压及心率. 结果显示,莫索尼定剂量依赖性地降低RVLM 神经元放电率,血压和心率. 莫索尼定10, 50 μg·kg^-1使放电率分别减少23% 和41%. 动脉注射选择性I₁-咪唑啉受体阻断剂依法克生10 μg·kg^-1, 可完全拮抗莫索尼定10 μg·kg^-1 的作用. 结果提示, 莫索尼定通过激动延髓腹外侧头端区神经元上的I₁-咪唑啉受体,抑制其自发放电活动.     

孤束核微注射内皮素-1对高血压大鼠心血管活动的影响

目的研究内皮素－１（ＥＴ－１）在孤束核对高血压大鼠心血管活动的作用。方法乌拉坦麻醉大鼠单侧孤束核微注射ＥＴ－１或ＥＴ受体拮抗剂后，观察血压、心率、左室收缩压和±ｄｐ／ｄｔｍａｘ的变化。结果在乌拉坦麻醉的ＷＫＹ大鼠和自发性高血压大鼠（ＳＨＲ），单侧孤束核微注射１．０ｐｍｏｌ或３．３ｐｍｏｌ的ＥＴ－１均可引起血压、左室收缩压和±ｄｐ／ｄｔｍａｘ升高，呈剂量依赖性；心率轻度减慢，与剂量不相关。血压持续升高９０ｍｉｎ以上。ＳＨＲ的心血管反应强度与ＷＫＹ大鼠无显著差异。孤束核微注射非选择性ＥＴＡ／ＥＴＢ受体拮抗剂ＰＤ１４２８９３对ＳＨＲ和ＷＫＹ大鼠的血压和心率均无明显影响。结论孤束核ＥＴ－１与ＳＨＲ的血压增高无关     

Blood pressure responses of endothelin-1 1-31 within the rostral ventrolateral medulla through conversion to endothelin-1 1-21

Endothelin-1 1-31 (ET-1 1-31), a novel member of the endothelin family comprising 31 amino acids and derived from the selective hydrolysis of big ET-1 by chymase, directly activates endothelin receptors or converts to ET-1 1-21 by ET converting enzyme (ECE). The cardiovascular effects of central ET-1 1-31 are not identified. The present study was designed to investigate the cardiovascular actions of ET-1 1-31 within the rostral ventrolateral medulla (RVLM) in anesthetized rats. Bilateral injection of ET-1 1-31 (0.5, 1, and 2 pmol for each side) into the rostral ventrolateral medulla produced an initial pressor and/or a long-lasting hypotensive action but did not affect HR. Unilateral microinjection of 2 and 4 pmol of ET-1 1-31 into the rostral ventrolateral medulla only produced a significant (P < 0.05) transient increase in blood pressure by an average of 13 and 12 mm Hg, respectively, whereas unilateral microinjection of 8 pmol of ET-1 1-31 produced a sustained fall in blood pressure (from 92 +/- 6 to 69 +/- 8 mm Hg, P < 0.05). The transient pressor effect of unilaterally injecting ET-1 1-31 (4 pmol) into the rostral ventrolateral medulla was completely abolished by pretreatment with either ETA receptor antagonist BQ123 (83 +/- 2 versus 84 +/- 5 mm Hg, P > 0.05) or ET converting enzyme inhibitor phosphoramidon (99 +/- 5 versus 99 +/- 7 mm Hg, P > 0.05) but not ETB receptor antagonist IRL1038 (89 +/- 6 versus 96 +/- 7 mm Hg, P < 0.05). In addition, prior injection of phosphoramidon also completely abolished the long-lasting hypotension of intra-RVLM ET-1 1-31 (8 pmol) but did not modify the depressor action of intra-RVLM ET-1 1-21 (from 100 +/- 6 to 76 +/- 8 mm Hg, P < 0.05). In conclusion, the current results suggest that the cardiovascular effects of intra-RVLM ET-1 1-31 might be the result of conversion of ET-1 1-31 to ET-1 1-21 through activation of ETA receptors.     

氯胺酮对大鼠头端延髓腹外侧区前交感神经元的作用(英文)

目的:研究氯胺酮在中枢交感心血管活动中的调节作用。方法:在25只氨基甲酸乙酯麻醉、三碘季铵酚制动并人工通气的雄性SD大鼠中,共细胞外记录到32个头端延髓腹外侧区前交感神经元的自发放电,这些神经元具有压力敏感性和向脊髓投射的特点。观察选择性NMDA受体拮抗剂氯胺酮对前交感神经元放电的影响。结果:静脉注射不同剂量的氯胺酮(3,6,12mg/kg)能增加RVLM前交感神经元的放电频率,同时能阻断这些神经元的压力敏感性,且具有剂量依赖性的特点。结论:氯胺酮通过阻断RVLM前交感神经元压力感受反射的紧张性抑制,从而调节交感心血管活动。     

Role of excitatory amino acid inputs to the rostral ventrolateral medulla in cardiovascular regulation

1. Excitatory amino acid (EAA)-mediated neural transmission in the rostral ventrolateral medulla (RVLM) is important for many cardiovascular reflexes, although the receptor subtypes involved vary depending on the specific response. 2. Although injection of the EAA ionotropic receptor antagonist kynurenic acid into the RVLM has no effect on baseline arterial pressure, this lack of effect appears to result from EAA inputs to RVLM exciting both excitatory and inhibitory mechanisms within the RVLM. 3. The balance between EAA-mediated excitation and inhibition of RVLM neurons may be shifted to excitation in experimental models of hypertension. 4. The excitatory influence that EAA inputs to the RVLM have on vasomotor neurons in the RVLM may involve a sarthran-sensitive intermediary in the RVLM.     

Efectsofmoxonidineinjectedintorostralventrolateralmedulaonbloodpressure,heartrate,andrenalsympatheticnerveactivityinrats

目的：观察延髓腹外侧头端（ＲＶＬＭ）注射莫索尼定（Ｍｏｘ）对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）及肾交感神经放电（ＲＳＮＡ）的影响．方法：麻醉大鼠ＲＶＬＭ注射１μＬＭｏｘ１，１０，１００μｍｏｌ·Ｌ－１，同步记录ＢＰ，ＨＲ及ＲＳＮＡ．结果：Ｍｏｘ１，１０，１００μｍｏｌ·Ｌ－１分别使ＢＰ从１３９±１０ｋＰａ降至１３０±１７ｋＰａ（Ｐ＜００５），１３８±１８ｋＰａ至１１４±１５ｋＰａ（Ｐ＜００１），ａｎｄ１３９±１９ｋＰａ至９４±１７ｋＰａ（Ｐ＜００１）．Ｍｏｘ不影响ＨＲ．Ｍｏｘ１μｍｏｌ·Ｌ－１增加ＲＳＮＡ５０％（Ｐ＜００５），１０μｍｏｌ·Ｌ－１对ＲＳＮＡ无影响（Ｐ＞００５），１００μｍｏｌ·Ｌ－１则降低ＲＳＮＡ２３％（Ｐ＜００５）．在缓冲神经切断大鼠，Ｍｏｘ１０μｍｏｌ·Ｌ－１抑制ＲＳＮＡ５０％（Ｐ＜００５），明显不同于缓冲神经完整的动物（Ｐ＜００１）．结论：麻醉大鼠ＲＶＬＭ注射Ｍｏｘ可降低ＢＰ，但不影响ＨＲ，且ＲＳＮＡ变化与其降压作用并不平行     

Opioid signalling in the rat rostral ventrolateral medulla

1. The present article reviews several aspects of opioid signalling in the rostral ventrolateral medulla (RVLM) and their implications for the neural control of blood pressure. 2. In the RVLM, preproenkephalin (PPE) mRNA is expressed by bulbospinal cells that are strongly barosensitive. These putative presympathetic neurons includes C1 and non-C1 neurons. 3. In the RVLM, PPE mRNA is also present in GABAergic neurons that do not project to the thoracic spinal cord. 4. Rostral ventrolateral medulla presympathetic cells receive enkephalinergic inputs and express mu-opioid receptors (MOR). Some of their synaptic inputs also contain MOR. 5. Pre- and post-synaptic modulation of RVLM presympathetic neurons by MOR agonists has been demonstrated in slices of neonate brain. The post-synaptic effect is inhibitory (increased gK). Presynaptic effects include disfacilitation (reduction of glutamate release) and possibly dishinhibition (reduction of GABA release). 6. In conclusion, opioid signalling plays a pervasive role in the medullospinal network that controls sympathetic tone and arterial pressure. Opioid peptides are made by the presympathetic, presumably excitatory, cells of the RVLM and by local GABAergic inhibitory neurons. In addition, RVLM presympathetic neurons are also controlled by opioid peptides at the pre- and post-synaptic level. mu-Opioid receptors are found post-synaptically, whereas presynaptic receptors probably include both mu and delta subtypes. Conditions that trigger the release of opioid peptides by presympathetic neurons or by inputs to these cells are not fully understood and may include decompensated haemorrhage and certain types of peripheral sensory stimulation related to acupuncture.     

RU486对硫酸皮质酮引起的头端延髓腹外侧区心血管神经元作用的影响

目的研究糖皮质激素（ＧＣ）的非基因组机制在交感神经活动调节中的作用。方法细胞外记录氨基甲酸乙酯麻醉的ＳＤ大鼠头端延髓腹外侧区（ＲＶＬＭ）被鉴定的心血管神经元的自发放电,观察微电泳硫酸皮质酮（Ｏ３ＲＴ对心血管神经元活动的影响,及其 ＧＣ受体拮抗剂 ＲＵ ４８６对ＣＯＲＴ导致神经元作用的影响。结果在ＲＶＬＭ共记录到３３个心血管神经元,微电泳硫酸皮质酮（ＣＯＲＴ）后２５（７６％）个神经元放电迅速加快,且具有剂量依赖性,余８个（２７％）心血管神经元自发放电没有变化;其中被ＣＯＲＴ兴奋的１２个单位微电泳ＲＵ４８６（糖皮质激素受体阻断剂）后神经元的基础放电没有明显变化（Ｐ＞０．０５）,但能部分（９个单位）或完全（３个单位）阻断硫酸皮质酮导致的兴奋作用。结论Ｏ３ＲＴ对ＲＶＬＭ心血管神经元具有快速的兴奋作用,ＲＵ４８６并不改变ＲＶＬＭ心血管神经元的基础活动,但能部分或完全阻断ＣＯＲＴ导致的神经元兴奋作用。     

Functions of angiotensin peptides in the rostral ventrolateral medulla

1. It was first shown several years ago that the rostral part of the ventrolateral medulla (VLM) contains a high density of receptor binding sites for angiotensin II (AngII). In the present paper we briefly review recent studies aimed at determining the actions of both exogenous and endogenous angiotensin peptides in the rostral VLM, as well as their specific sites of action. 2. The results of these studies have shown that angiotensin peptides can excite pressor and sympathoexcitatory neurons in the rostral VLM, but do not appear to affect non-cardiovascular neurons in this region. 3. It is known that pressor neurons in the rostral VLM include both catecholamine and non-catecholamine neurons. There is evidence that, at least in conscious rabbits, both of these types of neurons are activated by AngII. The specific endogenous angiotensin peptide or peptides that affect pressor neurons in the rostral VLM have not yet been definitively identified. 4. It is also possible that different angiotensin peptides may have different effects on pressor neurons in the rostral VLM, mediated by different receptors. Further studies will be needed to define these different functions as well as the specific receptors and cellular mechanisms that subserve them.