莫索尼定对麻醉大鼠颈动脉窦压力感受器反射的影响

目的:观察莫索尼定对颈动脉窦压力感受器反射的影响。方法:利用灌流左颈动脉窦方法,观察莫索尼定对麻醉大鼠压力反射机能参数的影响。恒流灌流股动脉,记录灌流压变化,确定莫索尼定对血管阻力的影响。结果:莫索尼定32,100μmol·L~(-1)使颈动脉窦压力反射机能曲线向右上移位,曲线最大斜率和反射性平均动脉压下降幅度均减小,提示莫索尼定对压力感受器反射有抑制作用。伊法克生100μmol·L~(-1)完全阻断莫索尼定100μmol·L~(-1)的效应。莫索尼定显著增加血管阻力。结论:莫索尼定对颈动脉窦压力反射有直接抑制作用,此作用可能在于其引起窦壁收缩所致。     

白藜芦醇抑制麻醉大鼠颈动脉窦压力感受性反射(英文)

目的研究白藜芦醇的心血管保护作用是否与其对颈动脉窦压力感受器的作用有关。方法隔离灌流麻醉大鼠颈动脉窦区,同时记录动脉血压的变化,并绘制压力感受性反射的功能曲线。结果白藜芦醇(30,60和120μmol.L-1)隔离灌流颈动脉窦区,压力感受性反射机能曲线向右上方移位,曲线的最大斜率下降,反射性血压下降的幅度降低,阈压增加,其变化呈浓度依赖性。预先应用NO合酶抑制剂L-NAME100μmo.lL-1或钙通道开放剂BayK8644500nmol.L-1可消除白藜芦醇对压力感受器的抑制作用。用酪氨酸磷酸酶抑制剂正钒酸钠1mmol.L-1预处理对白藜芦醇抑制压力感受性反射的作用无影响。结论白藜芦醇对大鼠颈动脉窦压力感受器反射有抑制作用,此作用可能与局部NO的释放及减弱牵张敏感性通道的钙离子内流有关。     

17β-雌二醇抑制麻醉雄性大鼠颈动脉窦压力感受器的活动(英文)

目的:观察17β-雌二醇对颈动脉窦压力感受器活动的影响。方法:在麻醉雄性大鼠隔离灌流颈动脉窦条件下记录窦神经传入放电,观察17β-雌二醇(E_2)对压力感受器机能曲线和机能参数的影响。结果:E_23,10和30μmol/L使压力感受器机能曲线向右下方移位,曲线最大斜率和窦神经传入放电积分最大值均明显减小,表明E_2可抑制颈动脉窦压力感受器活动。雌激素受体抑制剂他莫昔芬10μmol/L不能阻断E_2的效应。一氧化氮合酶阻断剂L-NAME100μmol/L完全阻断E_2对压力感受器活动的抑制效应。一氧化氮供体SIN-1 10μmol/L能加强E_2的效应。结论:E_2抑制雄性大鼠颈动脉窦压力感受器的活动,此效应系其使内皮细胞释放一氧化氮所致。     

白藜芦醇对麻醉大鼠颈动脉窦压力感受器的作用

在隔离灌流左侧颈动脉窦区的麻醉大鼠上观察了白藜芦醇对颈动脉窦压力感受器活动的影响。隔离灌流麻醉大鼠的颈动脉窦区，同时记录窦神经放电，并绘制压力感受器活动的机能曲线。白藜芦醇(30， 60及120 μmol·L^-1)隔离灌流颈动脉窦区时，压力感受器活动的机能曲线向右下方移位，曲线的斜率以及窦神经放电的最大积分值显著下降，且其变化呈一定的剂量依赖性。预先应用NO合酶抑制剂(L-NAME， 100 μmol·L^-1)可完全消除白藜芦醇对压力感受器活动的抑制作用；预先应用钙通道的开放剂(Bay K8644， 500 nmol·L^-1)可以取消白藜芦醇的抑制作用；预先应用正矾酸钠(sodium orthovanadate， 1 mmol·L^-1)后，对白藜芦醇抑制压力感受器活动的作用无影响。白藜芦醇对大鼠颈动脉窦压力感受器活动有抑制作用，此作用可能与局部NO的释放及减弱牵张敏感性通道介导的钙离子内流有关。     

胍丁胺抑制麻醉大鼠颈动脉窦压力反射(英文)

目的:观察胍丁胺对颈动脉窦压力感受器反射的影响。方法:利用灌流左颈动脉窦方法,观察胍丁胺对麻醉大鼠压力反射机能参数的影响。结果:(1)胍丁胺1,5,10mmol/L均使颈动脉窦压力反射机能曲线向右上方移位,曲线最大斜率和反射性平均动脉压下降幅度均减小,提示胍丁胺对压力感受器反射有抑制作用;(2)预先应用咪唑啉受体(IR)和肾上腺素能α_2受体(α_2-AR)拮抗剂咪唑克生(idazox-an,0.1mmol/L),则可完全阻断胍丁胺5mmol/L的效应。预先应用α_2受体拮抗剂育亨宾(yohimbine,15μmol/L),则可部分阻断其效应;(3)预先应用NOS抑制剂L-NAME(500μmol/L),对胍丁胺的抑制作用无影响。结论:胍丁胺对颈动脉窦压力反射有抑制作用,并由咪唑啉受体和α_2受体介导。     

八肽胆囊收缩素对大鼠颈动脉窦神经传入放电的抑制作用(英文)

目的　观察八肽胆囊收缩素 (CCK 8)是否通过直接抑制颈动脉窦压力感受器放电活动而影响心血管功能。方法　在麻醉雄性大鼠隔离灌流颈动脉窦区条件下记录窦神经传入放电及积分。结果　①CCK 80 .1,0 .5和 1.0 μmol·L- 1使压力感受器机能曲线向右下方移位 ,曲线最大斜率和窦神经传入放电积分最大值均明显减小 ,表明CCK 8可剂量依赖性抑制颈动脉窦压力感受器活动。②预先灌流CCK 8非特异性受体阻断剂丙谷胺 10 0 μmol·L- 1或钙通道开放剂BayK86 440 .5 μmol·L- 1可部分阻断CCK 80 .5 μmol·L- 1对颈动脉窦压力感受器放电活动的抑制作用。预先灌流一氧化氮合酶抑制剂L NAME不能阻断CCK 8的效应。结论　CCK 8可直接抑制大鼠颈动脉窦压力感受器传入神经放电活动。其机制可能为CCK 8作用于颈动脉窦区相应的受体后 ,对牵张敏感性通道产生抑制作用。     

前列腺素对肾性高血压兔颈动脉窦压力感受器反射的影响

孤离颈动脉窦．记录腰交感神经活动．研究前列腺素对肾性高血压兔颈动脉窦压力感受器反射的影响。结果表明：①环加氧酶抑制剂消炎痛可使正常动物窦反射明显减弱，而对高血压动物却无明显作用。提示内源性前列腺素对正常动物窦反射起增强作用，而在高血压动物，这种作用缺失。②与正常动物相同．外源性前列环素（ＰＧＩ２）也使高血压动物窦反射明显增强，提示高血压动物动脉压力感受器对前列腺素的反应性仍保持正常，内源性前列腺素对高血压动物窦压力感受器反射无明显调制作用，主要可能由于内源性前列腺素（如ＰＧＩ２）缺乏所致。     

钩藤碱对麻醉大鼠颈动脉窦压力感受器活动的抑制作用(英文)

目的探讨钩藤碱(Rhy)对大鼠颈动脉窦压力感受器活动的影响及其有关机制。方法通过隔离灌流颈动脉窦区的方法来获得颈动脉窦压力感受器活动的各项参数,阈压(TP)、饱和压(SP)、最大斜率(PS)和窦神经放电的最大积分值(PIV)。① Rhy10, 50和100μmo·lL-1用K-H液稀释后,隔离灌流颈动脉窦区。待钩藤碱发挥作用后,用K-H液冲洗恢复,在给药前后以阶梯方式升降窦内压以刺激颈动脉窦压力感受器,同时记录窦神经传入放电及积分。②分别预先灌流一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(L-NAME)、K+通道阻断剂四乙胺(TEA)和L-钙通道开放剂Bay K8644,观察他们对钩藤碱效应的影响。结果①Rhy 10μmol.L-1灌流隔离的颈动脉窦区,PS从(19.2±0.3)%降至(18.2±0.1)%·kPa-1,PIV从(219.3±3.3)%降至(199.1±3.8)%,同时TP和SP分别从(8.2±0.3)和(21.5±0.1)增加至(9.1±0.1)kPa和(22.1±0.1)kPa。用Rhy 50和100μmol·L-1进行灌流时,如PS,TP和SP的变化均呈浓度依赖性,表明Rhy可以抑制CBA。②预先灌流L-NAME不能阻断Rhy的效应。③预先灌流K+通道阻断剂TEA 1mmol·L-1也不能阻断Rhy对颈动脉窦压力感受器放电活动的抑制。④预先灌流L-钙通道开放剂Bay K8644可大部分阻断Rhy的作用。结论 Rhy可直接抑制大鼠颈动脉窦压力感受器传入神经放电活动,其机制可能为Rhy抑制了动脉压力感受器上的Ca2+内流。     

莫索尼定对大鼠血管功能的影响

目的观察莫索尼定对自发性高血压大鼠(SHR)及正常大鼠血管功能的影响。方法制备离体大血管平滑肌条,将其固定于灌流肌槽中,记录离体大血管平滑肌条张力变化。测定莫索尼定对氯化钾(Kcl)诱发的离体大血管肌条的收缩反应的影响。结果在加入莫索尼定后的基础上,Kcl引起离体血管收缩效应明显减弱(P<0.05)。结论表明莫索尼定对二种大鼠的血管收缩均有抑制效应,具有降低外周阻力的功能。     

孤束核组胺能受体参与应激大鼠颈动脉窦压力感受性反射的重调定

目的 探讨孤束核(NTS)组胺(HA)能受体是否影响应激对颈动脉窦压力感受性反射(CSR)的重调定。方法 应激一周的大鼠，麻醉后孤离双侧颈动脉窦区，将不同窦内压(ISP)与其对应的平均动脉压(MAP)值进行Logistic五参数曲线拟合，求得ISP-MAP关系曲线及特征参数，观察NTS注射不同HA受体拮抗剂对CSR的影响。结果 应激导致ISP-MAP关系曲线显全面上移，反射参数中阈压、饱和压、调定点和最大增益时ISP值增大，MAP反射变动范围及最大增益减小；NTS内注射H1或H2受体拮抗剂(氯苯吡胺，CHL，0．5／μg或西咪替丁，CIM，1．5μg)20min内均可明显减弱应激对CSR的上述改变，CIM减弱作用不如CHL；NTS内注射CHL或CIM后，均不能使应激的CSR水平完全恢复到相应的非应激对照水平。结论 应激引起CSR重调定，反射敏感性下降；部分机制可能是激活中枢HA能系统，NTS的H1和H2尤其H1受体在应激引起CSR重调定的机制中发挥重要作用；下丘脑-NTS的HA能通路可能是应激所致CSR重调定的下行通路之一。     

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     

Capsaicin facilitates carotid sinus baroreceptor activity in anesthetized rats

AIM: To study the effect of capsaicin on carotid sinus baroreceptor activity (CBA). METHODS: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid sinus baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized rats with perfused isolated carotid sinus. RESULTS: Low-concentration of capsaicin (0.2 μmol/L) had no significant effect on CBA, while perfusion of the isolated carotid sinus with middle-concentration of capsaicin (1 μmol/L) could shift FCCB to the left and upward, with peak slope (PS) increased from (2.47 %±0.14 %)/mmHg to (2.88 %±0.10 %)/mmHg (P<0.05) and peak integral value of carotid sinus nerve discharge (PIV) enhanced from 211 %±5 % to 238 %±6 % (P<0.01). The threshold pressure (TP) and saturation pressure (SP) were significantly decreased from 68.0±1.1 to 62.7±1.0 mmHg (P<0.01) and from 171.0±1.6 to 165.0±0.6 mmHg (P<0.01). By perfusing with high-concentration of capsaicin (5μmol/L), FCCB was shi     

Hydrogen sulfide facilitates carotid sinus baroreflex in anesthetized rats

AIM: To study effects of hydrogen sulfide (H2S) on the carotid sinus baroreflex (CSB). METHODS: The functional curve of the carotid sinus baroreflex was measured by recording changes in arterial pressure in anesthetized male rats with perfused carotid sinus. RESULTS: H2S (derived from sodium hydrosulfide) at concentrations of 25, 50, and 100 micromol/L facilitated the CSB, shifting the functional curve of the baroreflex downward and to the left. There was a marked increase in peak slope (PS) and reflex decrease in blood pressure (RD). Effects were concentration-dependent. Pretreatment with glibenclamide (20 micromol/L), a K(ATP) channel blocker, abolished the above effects of H2S on CSB. Pretreatment with Bay K8644 (an agonist of calcium channels; 500 nmol/L) eliminated the effect of H2S on CSB. An inhibitor of cystathionine gamma-lyase (CSE), DL-propargylglycine (PPG; 200 micromol/L), inhibited CSB in male rats and shifted the functional curve of the baroreflex upward and to the right. CONCLUSION: These data suggest that exogenous H2S exerts a facilitatory role on isolated CSB through opening K(ATP) channels and further closing the calcium channels in vascular smooth muscle. Endogenous H2S may activate the activity of the CSB in vivo.     

Urotensin Ⅱ inhibits carotid sinus baroreflex in anesthetized male rats

AIM: To study the effects of urotensin II (UII) on the carotid sinus baroreflex (CSB). METHODS: The functional curve of carotid sinus baroreflex was measured by recording changes in arterial pressure in anesthetized male rats with perfused isolated carotid sinus. RESULTS: UII at the concentration of 3 nmol/L had no effect on the CSB, while at the concentration of 30, 300 and 3000 nmol/L inhibited the CSB, shifting the functional curve of the baroreflex upward and to the right. There was a marked decrease in peak slope and reflex decrease in blood pressure. These effects of UII were concentration-dependent. Pretreatment with verapamil (an antagonist of the L-type calcium channel, 10 micromol/L) partially eliminated the above effects of UII (300 nmol/L) on the CSB. Pretreatment with BIM-23127 (3 micromol/L), an antagonist of human and rat UII receptors, abolished the actions of UII on the CSB. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) 100 micromol/L did not affect the inhibitory effects of UII (300 nmol/L) on the CSB. CONCLUSION: These data suggest that UII exerts an inhibitory action on the isolated CSB. Such an action of UII is predominantly mediated by the UII receptors in vascular smooth muscles, resulting in the opening of L-type calcium channels.     

Effect of naloxone on baroreflex, sympathetic tone and blood pressure in the cat

Studies were designed to determine the effect of naloxone on sympathetic nerve activity and blood pressure and, also to investigate the central effect of naloxone in relation to the baroreflex system in -chloralose-anesthetized cats. Following intravenous injection of naloxone (2 mg/kg), preganglionic splanchnic nerve (PSN) activity significantly increased in parallel to the increase in blood pressure. Set gain (mmHg⁻¹) of carotid sinus baroreflex together with the operational range (mmHg) was increased after naloxone. Intraventricular (4th) injection of naloxone (0.2 mg/kg) produced identical responses in blood pressure and PSN activity as well as an altered set gain and range of the baroreflex. Additionally, the pressor response to carotid hypotension and medullary pressor area stimulation were augmented during naloxone activation but not the pressor response to posterior hypothalamus stimulation. The depressor responses to stimulation of both carotid sinus nerve and medullary depressor region were facilitated by naloxone. These data suggest that naloxone has an effect on the central autonomic blood pressure regulatory circuits which participate in the carotid sinus baroreflex system.