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1.
银杏内酯B对离体大鼠胸主动脉收缩活动的影响   总被引:1,自引:0,他引:1  
目的:研究银杏内酯B对大鼠离体胸主动脉血管环收缩活动的影响.方法:采用离体血管灌流的方法,观察银杏内酯B对不同浓度氯化钾、去甲肾上腺素引起的大鼠胸主动脉收缩反应的影响,以收缩率为指标.结果:银杏内酯B高浓度(0.1 g·L-1)和中浓度(0.03 g·L-1)对KCl(60 mmol·L-1)引起的胸主动脉收缩具有拮抗作用(P<0.05,P<0.01),并能使20 mmol·L-1~60 mmol·L-1氯化钾对胸主动脉的收缩作用减弱或明显减弱(P<0.05,P<0.01);银杏内酯B高浓度(0.1 g·L-1)和中浓度(0.03 g·L-1)对去甲肾上腺素(10-5 mol·L-1)引起的大鼠胸主动脉收缩具有拮抗作用(P<0.05,P<0.01),并能使0.1~10 μmol·L-1 NE对胸主动脉的收缩作用减弱或明显减弱(P<0.05,P<0.01).结论:银杏内酯B对氯化钾、去甲肾上腺素引起的大鼠离体胸主动脉血管环收缩活动有明显拮抗作用.  相似文献   

2.
瓜萎提取物对离体家兔胸主动脉条收缩的影响   总被引:6,自引:0,他引:6  
以兔离体主动脉条为实验材料,观察EFT对去甲肾上腺素(NE)、氯化钾(KCl)和氯化钙(CaCl2)的剂量0交应曲线的影响及主动脉条的α受体及β受体的作用。观察了EFT对NE引起的兔主动脉条2种收缩成分的影响。结果EFT能舒张已被氯化钙、高钾和去甲肾上腺素收缩的兔主动脉条,使NE、KCl、CaCl2的剂量-效应曲线非平行右移,最大效应降低。EFT松驰血管平滑肌的作用不依赖于阻断α受体或β受体。而与  相似文献   

3.
本文观察了海洋硫酸多糖DPS对去甲肾上腺素(NA)和氯化钾(KCl)所致大鼠主动脉环收缩反应的影响。结果表明,DPS 1mg·L-1能抑制NA和KCl所致大鼠主动脉环收缩,使量效反应曲线非平行性右移,压低最大反应曲线,显示DPS对NA和KCl所致大鼠主动脉环收缩具有非竞争性拮抗作用。提示,DPS有抑制电压依赖性Ca2+通道和受体活化性Ca2+通道的作用。  相似文献   

4.
薤白提取物对兔离体主动脉条的作用   总被引:1,自引:0,他引:1  
本实验以离体兔主动脉条为标本 ,对薤白 (EA)的扩血管机制进行了探讨 .观察了薤白对去甲肾上腺素 (NE)、氯化钾 (KCl)和氯化钙 (CaCl2 )的剂量 效应曲线的影响及主动脉条的α受体及 β受体的作用 .观察了EA对NE引起的兔主动脉条两种收缩成分的影响 .结果表明EA能舒张已为氯化钙、高钾和去甲肾上腺素收缩的兔主动脉条 ,使NE、KCl、CaCl2 的剂量 效应曲线非平行右移 ,最大效应降低 .EA松弛血管平滑肌的作用不依赖于阻断α受体或 β受体 ,而与戊脉安 (Ver)相似 ,是通过阻断钙通道实现的 .但它们阻断钙通道的方式不同 .EA可能无选择性阻断电位依赖性钙通道和受体操纵性钙通道 .因此EA的扩血管机制与其对钙通道阻断作用有关 .  相似文献   

5.
双氢杨梅树皮素对兔胸主动脉条平滑肌收缩反应的影响   总被引:33,自引:0,他引:33  
用兔胸主动脉条研究双氢杨梅树皮素对去甲肾上腺素,KCl和CaCl2所致兔胸主动脉条收缩反应量效曲线的影响。双氢杨梅树皮素能显著地抑制NE,KCl和CaCl2所致兔胸主动脉条的收缩,量效曲线右移,最大反应降低,对高K^+兔胸动脉条收缩的抑制作用明显大于NE所致兔胸主动脉条收缩的抑制作用。  相似文献   

6.
目的:考察米非司酮对胰岛素抵抗高血压大鼠血管收缩功能的影响。方法:将40只雄性sD大鼠随机分为正常组、模型组、罗格列酮(O.4mg·kg-1)组、米非司酮低剂量(20mg·kg-1)组、米非司酮高剂量(40mg·kg-1)组。除正常组外均予以高脂饮食饲养,8周后,取血样测定各组大鼠空腹胰岛素含量、空腹血糖含量,并计算胰岛素敏感指数及抵抗指数以判断胰岛素抵抗模型是否形成,测定血清皮质酮浓度以考察胰岛素抵抗形成过程中糖皮质激素的变化,测定。肾上腺素和去甲肾上腺素浓度以考察交感神经紧张程度,并于实验期间采用套尾法每4周测定1次血压。实验8周末处死大鼠,取出胸主动脉,制备胸主动脉环。用氯化钾预刺激收缩血管环后,分别加入系列浓度的去甲肾上腺素(1X10^-1x10^-5mol·L-1)和血管紧张素Ⅱ(1×10^8、3×10^-8×10^-7、3×10 ^-7和1×10^-6 mol·L-1),并在地塞米松孵育后再次加入同等系列浓度的去甲肾上腺素。采用生物机能实验系统测定胸主动脉血管的收缩幅度,以氯化钾诱发的最大收缩幅度为100%,将加入去甲肾上腺素或血管紧张素Ⅱ后的血管收缩幅度与氯化钾诱发的最大收缩幅度之间的百分比计为收缩率以反映血管收缩功能。结果:高脂饮食饲养8周可致动物出现高血糖、高胰岛素血症、胰岛素敏感性降低、胰岛素抵抗指数上升,以及血清儿茶酚胺、血清皮质酮水平和血压升高,米非司酮可逆转除皮质酮水平升高以外的上述变化。与正常组相比,模型组大鼠胸主动脉环对去甲肾上腺素及血管紧张素Ⅱ的收缩反应明显增强;与模型组相比,米非司酮高、低剂量组大鼠胸主动脉环对去甲肾上腺素及血管紧张素Ⅱ所致的收缩反应显著降低,用地塞米松孵育后,其对去甲肾上腺素所致的收缩反应与模型组相比无显著变化,但较正常组及未用地塞米松孵育时显著升高。结论:高脂饮食饲养8周可诱导大鼠形成胰岛素抵抗高血压模型并伴有血管收缩功能障碍;米非司酮可改善以上症状,推测其可能通过拮抗糖皮质激素的生物学效应及降低胰岛素抵抗高血压大鼠血管环对血管紧张素Ⅱ的收缩性而发挥作用。  相似文献   

7.
N—甲基小檗胺扩血管作用原理的研究   总被引:2,自引:0,他引:2  
N—甲基小檗胺可非竞争性抑制氯化钾、氯化钙、去甲肾上腺素引起的家兔胸主动脉条收缩。其拮抗参数pD_(2’)分别为3.44、3.67和3.73。对去甲肾上腺素引起的外钙性收缩有抑制作用,对内钙性收缩无影响,说明其作用原理与拮抗钙离子内流有关。  相似文献   

8.
瓜蒌提取物对离体家兔胸主动脉条收缩的影响   总被引:10,自引:0,他引:10  
以兔离体主动脉条为实验材料,观察EFT对去甲肾上腺素(NE)、氯化钾(KCl)和氯化钙(CaCl2)的剂量-效应曲线的影响及主动脉条的α受体及β受体的作用.观察了EFT对NE引起的兔主动脉条2种收缩成分的影响.结果EFT能舒张已被氯化钙、高钾和去甲肾上腺素收缩的兔主动脉条,使NE、KCl、CaCl2的剂量-效应曲线非平行右移,最大效应降低.EFT松驰血管平滑肌的作用不依赖于阻断α受体或β受体.而与戊脉安(Ver)相似,是通过阻断钙通道实现的.但它们阻断钙通道的方式不同.EFT可能无选择性阻断电位依赖性钙通道和受体操纵性钙通道,而Ver则只选择性阻断.因此,EFT的扩血管机制与其对钙通道阻断作用有关  相似文献   

9.
目的研究不同动脉对同一血管收缩剂的反应性是否存在差异,及其与L-型钙通道的关系。方法采用离体血管张力测定实验方法,测定在累积浓度血管收缩剂处理下的大鼠胸主动脉、肾内动脉或冠状动脉的张力变化以及L-型钙通道阻断剂硝苯地平(nifedipine)的影响。结果苯肾上腺素(phenylephrine,Phe)对冠状动脉无明显影响,但可诱导胸主动脉和肾内动脉产生明显的浓度依赖性收缩,胸主动脉的pEC_(50)明显大于肾内动脉(P<0.05);给予硝苯地平孵育后,再给予累积浓度的Phe,胸主动脉收缩的下降幅度大于肾内动脉(P<0.05)。5-羟色胺(5-hydroxy tryptamine,5-HT)对胸主动脉的收缩作用不明显,但可浓度依赖性诱导肾内动脉和冠状动脉收缩;给予硝苯地平孵育后,再给予累积浓度的5-HT,冠状动脉收缩的下降幅度明显大于肾内动脉(P<0.05)。胸主动脉、肾内动脉和冠状动脉均对血栓素A2类似物(9,11-dideoxy-11α,9α-epoxymethanoprostaglandin,U46619)产生浓度依赖性收缩,肾内动脉收缩量效曲线的E_(max)最小(P<0.05),胸主动脉收缩量效曲线pEC_(50)最大(P<0.05)。给予硝苯地平孵育后,再给予累积浓度的U46619,冠状动脉收缩的下降幅度最大,胸主动脉收缩的下降幅度最小。结论大鼠胸主动脉、肾内动脉及冠状动脉对同一血管收缩剂的反应存在异质性,其中L-型钙通道介导的收缩作用也不同。  相似文献   

10.
目的 分析α1 肾上腺素受体阻断药多沙唑嗪手性对映体对兔胸主动脉和颈总动脉的选择性作用 ,以探讨作为良性前列腺增生症治疗药物的可能性。方法 测定去甲肾上腺素 (NE)诱发兔离体胸主动脉和颈总动脉收缩反应 ,并采用Schild作图法计算rac 多沙唑嗪、R 多沙唑嗪和S 多沙唑嗪的pA2 值。结果 在兔胸主动脉和颈总动脉 ,0 .0 3 ,0 .1和 0 .3μmol·L-1 的rac 多沙唑嗪、R 多沙唑嗪和S 多沙唑嗪均使NE诱发的血管收缩反应量效曲线平行右移 ,Emax不变 ;由Schild作图法计算得到的多沙唑嗪及其手性对映体的斜率值 ,经统计学分析符合竞争性拮抗。3种拮抗剂pA2 值的强度顺序为 :R 多沙唑嗪 >rac 多沙唑嗪 >S 多沙唑嗪。结论 与多沙唑嗪及其手性对映体对人前列腺组织作用的报道结果不同 ,S 多沙唑嗪对兔胸主动脉和颈总动脉α1 肾上腺素受体拮抗作用的选择性显著低于rac 多沙唑嗪和R 多沙唑嗪  相似文献   

11.
1. The effects of neuropeptide Y (NPY) on resistance arteries were investigated on 3rd generation mesenteric arterioles of the rat. 2. Contractions were elicited by noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha), depolarization (KCl substituted for NaCl) and by the calcium agonist Bay K 8644, in the absence and in the presence of NPY (100 nM), a concentration which by itself did not induce vasoconstriction. 3. NPY produced a leftward shift of the concentration-response curves to the agonists and to KCl, without any alteration of maximal contractions. 4. NPY also potentiated contractions elicited by addition of CaCl2 to KCl-depolarized vessels, but its effect on calcium-induced contractions decreased with increasing KCl concentrations (from 20 to 100 mM). 5. Calcium-induced contractions were inhibited by the calcium channel blocker nitrendipine, both in the presence and absence of NPY (100 nM). NPY increased slightly (but significantly) the sensitivity to nitrendipine (the apparent KB increased from 2.9 x 10(-10) M to 1.6 x 10(-10) M). 6. The KCl concentration necessary for the maximal effect of Bay K 8644 was decreased in the presence of NPY, and the sensitivity to the calcium channel agonist was increased. 7. Elevating the KCl concentration in the bath from 5 to 20 mM (which gives the same displacement to the left of the KCl concentration-effect curve seen in the presence of NPY) induced a parallel leftward shift of NA and 5-HT concentration-response curves. This shift was identical to the one induced by NPY on 5-HT-evoked contractions, but it was significantly smaller (P less than 0.001) than the shift of the NA concentration-response curve observed in the presence of NPY. In the latter case, NPY enhanced more markedly the contractions induced by low NA concentrations (between 10(-9) and 3 x 10(-8 M) than those induced by high concentrations (up to 3 x 10(-7) M), thus giving a shallow concentration-response curve. 8. The results strongly suggest that NPY partially depolarizes the arterioles and induces an increase in calcium entry through voltage-dependent channels, thus enhancing contractions elicited by agonists or by KCl-depolarization. In addition, they support the view that another mechanism also plays a part in the potentiation by NPY of the effects of low concentrations of NA.  相似文献   

12.
The effects of flurazepam and diazepam, benzodiazepine derivatives, on contractions (or contractures) induced by Ca++, K+ or norepinephrine were examined in the isolated canine coronary artery and thoracic aorta. Ca++-Induced contraction was evoked by cumulative addition of CaCl2 to Ca++-depleted K+-depolarizing solution; K+: and norepinephrine-induced contractions were evoked by cumulative addition of KCl and norepinephrine, respectively, to the medium. Flurazepam and diazepam (1 X 10(-5), 3 X 10(-5) and 1 X 10(-4) M for coronary artery; 3 X 10(-5) and 1 X 10(-4) M for thoracic aorta) shifted the dose-response curves for KCl downwards in a non-competitive manner, and shifted the dose-response curves for CaCl2 to the right in a competitive manner. Ca++-Induced contracture was inhibited completely by addition of flurazepam or diazepam (1 X 10(-4) M), and the inhibition was reversed dose-dependently by addition of CaCl2. Flurazepam and diazepam (3 X 10(-5) and 1 X 10(-4) M) shifted the dose-response curves for norepinephrine both rightwards and downwards in the thoracic aorta. These findings suggest that flurazepam and diazepam inhibit Ca++-influx into the cells (Ca++-antagonistic effect), causing relaxation and inhibition of K+-, Ca++-, or norepinephrine-induced contraction (or contracture) of the vascular smooth muscle.  相似文献   

13.
The vasodilator effect of eriodictyol (5,7,3',4'-tetrahydroxyflavanone), isolated previously from the medicinal plant Satureja obovata Lag., was studied in rat thoracic aorta rings. Eriodictyol relaxed in a concentration-dependent manner the noradrenaline (10(-6) M) and KCl (80 mM) induced contractions. The relaxant effect was more potent in noradrenaline precontracted preparations (IC50 = 6.11 +/- 0.2 x 10(-5) M) than in those precontracted with KCl (IC50 = 2.96 +/- 0.1 x 10(-4) M). Eriodictyol produced weakly concentration-dependent inhibition of the phasic component induced by KCl and noradrenaline while the inhibition of the tonic phase of these contractions was more pronounced. These effects were endothelium independent. In addition, eriodictyol (10(-5) and 5 x 10(-5) M) inhibited CaCl2 cumulative concentration response curves. Eriodictyol weakly inhibited the release of calcium from the sarcoplasmic reticulum and its contribution to the relaxant effect seems to be slight. We have also observed the relaxant effect of eriodictyol on phorbol-12-myristate-13-acetate (PMA) (10(-7) M) induced contractions both in normal calcium (IC50 = 4.69 +/- 0.3 x 10(-5) M) and calcium-free medium (IC50 = 3.74 +/- 0.4 x 10(-5) M). Finally we studied the effects on protein kinase C (PKC) activity. This flavonoid did not show any activity. These results suggest that the vasodilator effect of eriodictyol in rat thoracic aorta could be partially related to the inhibition of calcium influx or other enzymatic protein subsequent to activation of PKC related to the activation of contractile proteins like myosin light chain kinase (MLCK).  相似文献   

14.
马欣  李孝光 《药学学报》1989,24(10):786-788
硫酸锌是体内一种重要的微量元素,它使离体动物心脏动作电位振幅降低,有效不应期延长,并能显著降低家兔窦房结自律性。本文采用离体豚鼠胸主动脉条和犬门静脉环标本,观察硫酸锌对KCl,CaCl_2和去甲肾上腺素(NE)诱发血管平滑肌收缩的影响。进一步探讨硫酸锌与Ca~(2 )的作用关系。  相似文献   

15.
Effects of a Ca2+ channel facilitator, CGP 28,392, on smooth muscle contractions were examined in order to delineate characteristics of Ca2+ channels in rabbit and rat aortae and guinea-pig taenia caeci. Application of increasing concentrations of KCl induced contractile responses in these smooth muscles and CGP 28,392 shifted the concentration-response curve for KCl to the left. The maximum response was also increased in rat aorta and guinea-pig taenia. CGP 28,392 also shifted the concentration-response curves for noradrenaline in rat aorta and for histamine in taenia to the left and increased the maximum response in rat aorta. However, the corresponding curve for noradrenaline in rabbit aorta was not affected by CGP 28,392. The sustained contractions induced by KCl were inhibited by cumulative application of verapamil in these smooth muscles. Pretreatment of the muscle with CGP 28,392 decreased the inhibitory effect of verapamil. The noradrenaline-induced contraction in rat aorta and the histamine-induced contraction in taenia were also inhibited by verapamil, and CGP 28,392 antagonized the effect of verapamil. The noradrenaline-induced contraction in rabbit aorta was only slightly inhibited by verapamil, and CGP 28,392 did not modify the effect of verapamil. In these smooth muscles, cumulative application of Ca2+ to the Ca2+-depleted, KCl-treated muscle induced contraction, and the concentration-response curve for Ca2+ was shifted to the left by CGP 28,392 and to the right by verapamil. The concentration-response curves for Ca2+ in Ca2+-depleted, noradrenaline-treated rabbit and rat aortae and in Ca2+-depleted, histamine-treated taenia were also shifted to the left by CGP 28,392 and to the right by verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

16.
BTHP及吡那地尔对离体大鼠子宫平滑肌的作用   总被引:1,自引:0,他引:1  
苄基四氢巴马汀(BTHP)及吡那地尔(Pinacidil)对子宫平滑肌的作用研究结果如下:BTHP可使子宫平滑肌的收缩频率、幅度和张力均明显增强,而Pinacidil不仅可抑制或取消子宫的自发性节律性收缩.表现为明显的松弛作用.而且对BTHP所致的子宫收缩也有明显的拮抗作用。BTHP能增强氯化钾及催产素所致子宫的收缩反应.使收缩幅度加大.频率加快,张力提高.而Pinacidil则相反.表现为明显的抑制作用.使子宫松弛。BTHP可使高钾去极化子宫的CaCl2量效曲线左移、上移,而Pinacidil则使量效曲线右移.最大反应(Emax)不变。  相似文献   

17.
度洛西汀对大鼠胸主动脉环舒张功能的影响   总被引:2,自引:2,他引:0  
目的研究度洛西汀(DLX)对血管舒张功能的影响并探讨其作用机制。方法采用离体血管环灌流装置,观察DLX对大鼠胸主动脉环的作用及不同工具药的影响。结果 DLX对KCl(30 mmol.L-1)和NE(1μmol.L-1)预收缩的血管环具有浓度依赖的舒张作用,对内皮完整和去内皮血管环舒张作用无差异,该舒张作用为非内皮依赖性。在KCl预收缩基础上,加入钾通道阻断剂格列苯脲Gli(10μmol.L-1)、四乙胺TEA(10 mmol.L-1)、氯化钡BaCl2(1 mmol.L-1)、四氨基吡啶4-AP(1 mmol.L-1)和5-HT2受体阻断剂赛庚啶(1μmol.L-1)均不能抑制DLX的舒血管效应;α1受体阻断剂哌唑嗪(1μmol.L-1)组对DLX舒血管作用有抑制作用。在无钙液中,DLX可以明显抑制NE和CaCl2收缩血管的作用。结论 DLX能够浓度依赖性的舒张血管,其机制可能与抑制经由血管平滑肌细胞膜VDC和ROC通道的钙离子内流,拮抗α1受体以及抑制胞质内钙离子释放有关。  相似文献   

18.
The effects of chloroethylclonidine on alpha(1)-adrenoceptor-mediated contraction in endothelium-denuded caudal arteries and aorta from normotensive Wistar and Wistar Kyoto (WKY), and from spontaneously hypertensive (SHR) rats were evaluated. Chloroethylclonidine elicited concentration-dependent contractions. Maximal contraction was similar in caudal arteries among strains ( approximately 40% of noradrenaline effect). However, chloroethylclonidine elicited a higher contraction in aorta from SHR than from normotensive rats. In Wistar aorta chloroethylclonidine produced the smallest contractile response. In SHR aorta, BMY 7378 and 5-methylurapidil blocked chloroethylclonidine-elicited contraction, while (+)-cyclazocine did not inhibit it; while in caudal arteries, 5-methylurapidil blocked chloroethylclonidine action; the other antagonists had no effect. In chloroethylclonidine-treated aorta noradrenaline elicited biphasic contraction-response curves, indicating a high affinity (pD(2), 8.5 - 7.5) chloroethylclonidine-sensitive component and a low affinity (pD(2), 6.3 - 5.2) chloroethylclonidine-insensitive component. The high affinity component was blocked by chloroethylclonidine; while in caudal arteries noradrenaline elicited monophasic contraction-response curves with pD(2) values (6.5 - 5.7) similar to the low affinity component in aorta. Chloroethylclonidine inhibition of noradrenaline response was greater in aorta than in caudal arteries. Chloroethylclonidine increased the EC(50) values of noradrenaline approximately 1000 fold in aorta and approximately 10 fold in caudal arteries. In SHR aorta BMY 7378 protected alpha(1D)-adrenoceptors and in caudal arteries 5-methylurapidil protected alpha(1A)-adrenoceptors from chloroethylclonidine alkylation, allowing noradrenaline to elicit contraction. These results show marked strain-dependent differences in the ability of chloroethylclonidine to contract aorta; moreover, chloroethylclonidine stimulates alpha(1D)-adrenoceptors in aorta and alpha(1A)-adrenoceptors in caudal arteries. The higher contraction observed in aorta from SHR and WKY suggests an augmented number of alpha(1D)-adrenoceptors in these strains.  相似文献   

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