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1.
将大鼠置于模拟海拔8km高度的低压舱内缺氧1周及缺氧后空气中常氧恢复1周和2周,观察了左右心室功能、心肌肥厚、心肌收缩蛋白含量及其Ca ̄(2+),Mg ̄(2+)-ATP酶活性的动态变化。结果表明,8km缺氧1周后肺动脉压及右心室收缩压明显升高,左右心室±dp/dtmax及收缩指数明显降低。左右心室肌明显肥厚,心肌收缩蛋白Ca ̄(2+),Mg ̄(2+)-ATP酶活性明显减低。缺氧后常氧恢复1和2周后,左右心室功能逐渐恢复达到或接近正常水平,心肌肥厚逐渐减轻或恢复正常,心肌收缩蛋白Ca ̄(2+),Mg ̄(2+)-ATP酶活性也逐渐升高。因此说明:心肌收缩蛋白Ca ̄(2+),Mg ̄(2+)-ATP酶活性的改变是心功能变化的重要生化基础之一,它的减低是缺氧心肌对环境的代偿适应。  相似文献   

2.
本实验观察了正常及高血压大鼠红细胞膜Ca2+,Mg2+-ATP酶对不同浓度Ca2+及Mg2+的反应。结果表明:(1)在自发性高血压大鼠(SHR),此酶最适反应的Ca2+浓度为10-6mol/L;WKY大鼠为10-4mol/L;两肾一环型肾性高血压大鼠(RHR)为10-7mol/L,Wistar大鼠为10-4mol/L,Ca2+高于以上各相应浓度时该酶活性受到抑制;(2)作为该酶激动剂的Mg2+有其最适激活浓度,在WKY大鼠、RHR及Wistar大鼠均为4.5mol/L;(3)高浓度Mg2+(36.0mol/L)可以逆转高浓度Ca2+对该酶的抑制作用。以上结果表明,底物Ca2+浓度的变化对Ca2+,Mg2+-ATP酶的催化活性影响极大,该酶活性的促发及维持必须有适宜浓度的Mg2+。高血压时此酶对Ca2+的敏感性增高,且Mg2+对酶保护作用更为明显。本结果提示,胞内高浓度Ca2+不仅是高血压发生的原因之一,并可能与其发展及恶化有关。  相似文献   

3.
模拟5000m中度缺氧时,大鼠右室功能显著加强,而左室功能加强不显著;左右心室肌原纤维Ca2+,Mg2+-ATP酶活性下降,肌球蛋白同功酶V2和V3百分含量增加,V1百分含量减少。8000m重度缺氧时,右室功能减弱,但无统计学意义,左室功能减弱有显著性;ATP酶活性和同功酶的变化超过5000m组。此外,右室ATP酶活性与PAP呈反比且有显著性,左室ATP酶活性与CASP虽也呈反比但无显著性;右室同功酶V3百分含量与PAP呈正比,左室同功酶V3百分含量与CASP不呈比例。上述结果表明,因短期突发严重缺氧引起的心肌供氧不足对左心室心肌的直接损伤作用大于右心室心肌。  相似文献   

4.
用生物膜的拆离与重建技术,研究了Mg2+对阿霉素(Adriamycin,ADM)抑制猪心线粒体H+-ATP酶及其重建脂酶体(L·H+-ATP酶)活性的影响。用胆酸盐透析方法将H+-ATP酶在大豆磷脂脂质体上重建。实验结果表明,重建H+-ATP酶的ADM的敏感性较仅纯化而未重建者明显增加,这提示ADM的抑制作用依赖于磷脂。但是,在有Mg2+(1mmol/L)条件下重建的H+-ATP酶对ADM的敏感性较无Mg2+者却又显著降低,这提示Mg2+对ADM抑制线粒体H+-ATP酶的作用具有拮抗效应。Mg2+的这种拮抗效应是与其在透析重建H+-ATP酶过程中诱导脂酶体的磷脂的物理状态的改变相关的。所得实验结果对于阐明ADM抑制线粒体H+-ATP酶的作用机理与磷脂的相关性提供了较直接的实验证据。  相似文献   

5.
本研究探讨低氧和AlF-4等药物经G-蛋白敏感的跨膜信号通路对心血管肌源性张力的调控作用。在含有稳定表达Na+-Ca2+交换蛋白的CK1.4细胞中,用fura-2荧光影像确定细胞低氧对胞浆游离Ca2+[Ca2+]i的影响。在离体犬心乳头肌、颈动脉、主动脉及肺动脉恒温灌流样本中,用张力-电换能器测量低氧灌流和AlF-4等药物对心血管肌源性张力的影响。在整体犬体内,按拉丁方设计,用125Isod-1获得不同剂量VISA高效剂细胞内分布等药代动力学参数。结果表明:①在CK1.4细胞中,低氧抑制Na+-Ca2+交换蛋白,产生Ca2+内流,升高[Ca2+]i;②低氧灌流削弱AlF-4所致的血管收缩而明显易化Ca2+内流所致的心乳头肌收缩,与结果1)吻合;③VISA高效剂分布至细胞内,协同AlF-4,模拟并激活G-蛋白敏感的跨膜信号通路,显著改善低氧所致的Na+-Ca2+交换蛋白等跨膜大分子和心血管收缩蛋白氧化损害。  相似文献   

6.
神经节苷脂(Gangliosides)是红细胞膜Ca~(2+)-Mg~(2+)ATPase的一种激活剂,这种激活作用也是依赖于Ca~(2+)存在。在200μmol/LCa~(2+)存在的反应体系中,100μg/mLGangliosides对Ca~(2+)-Mg~(2+)ATPase的激活作用最大,为基本酶活性的150%以上。实验还发现CaM拮抗剂三氟拉嗪(TFP)、粉防已碱(Tet)等也同样抑制Gangliosides的这种激活作用。其抑制的IC_(50)值为25μmol/L和30μmo1/L;而此浓度下抑制剂存在的反应体系中,对Ca~(2+)-Mg~(2+)ATPase的基本活性影响不大。  相似文献   

7.
研究了镧、轧、镱及四种配合物对Ca~(2+)-ATP酶活性的影响.结果表明,低浓度的La~(3+),Gd~(3+)和Yb~(3+)对肌质网Ca~(2+)-ATP酶有激活作用;随着其浓度的增加,它们对酶活性的抑制程度增大;而La~(3+),Gd~(3+)和Yb~(3+)对纯化的Ca2~(+)-ATP酶则只有抑制作用;Gd─N─乙酰─缬氨酸和Yb─丙氨酰代丙氨酸配合物对肌质网膜和纯化的Ca~(2+)-ATP酶活性的影响与Gd~(3+)及Yb~(3+)类似,但其激活程度和抑制程度比Gd~(3+)及Yb~(3+)小;Gd─DTPA和Yb-DTPA对Ca2~(+)-ATP酶活性基本无影响。  相似文献   

8.
在有Ca2+和钙调蛋白存在时,肌球蛋白轻链激酶催化肌球蛋白磷酸化,促使肌动蛋白激活的肌球蛋白(肌动球蛋白)Mg2+-ATP酶活性显著增加.然而,肌球蛋白磷酸化水平与Mg2+-ATP酶之间的关系是非线性的,原肌球蛋白可以进一步增加Mg2+-ATP酶的活性,但仍不改变它们之间的非线性关系.肌球蛋白轻链激酶的合成肽抑制剂抑制了肌球蛋白磷酸化和Mg2+-ATP酶活性,并导致平滑肌去膜肌纤维的等长收缩张力与速度的降低.结果提示肌球蛋白轻链激酶参与脊椎动物平滑肌收缩的调节过程,肌球蛋白轻链磷酸化作用会引起平滑肌收缩  相似文献   

9.
稀土离子对CaM及Ca2+-Mg2+-ATPase活力及CD研究   总被引:4,自引:0,他引:4  
研究了稀土离子(Ln3+)对钙调蛋白(CaM)调控的Ca2+-Mg2+-ATPase的活力影响。结果表明,在CaM和Ca2+-Mg2+-ATPase的体系中,一些Ln3+(La3+、Gd3+)对由CaM调节的Ca2+-Mg2+-ATPase的活力影响呈现双相效应,即Ln3+在低浓度时,能提高激活Ca2+-Mg2+-ATPase的水解活力;在高浓度时,则抑制CaM调节Ca2+-Mg2+-ATPase活力的能力;少数Ln3+(Sm3+)仅表现出抑制效应。在无CaM的Ca2+-Mg2+-ATPase体系中,高浓度的Ln3+抑制Ca2+-Mg2+-ATPase的基础活力。结合圆二色(CD)谱信息对Ln3+和CaM相互作用的分子机制进行了初步的探讨。  相似文献   

10.
用TBA法测定了三尖杉酯碱的膜脂氧化效应;用纳秒荧光偏振技术研究了氧化膜脂对DPH标记大鼠心肌肌质网膜脂、ANM标记心肌肌质网Ca2+-ATPa功能及磷酸化微区运动状态的影响。随膜脂中氧化磷脂的增加,肌质网膜脂双层的微粘度增加,磷脂分子摆动角减小:DPH的荧光强度减弱,荧光寿命缩短。Ca2+-ATPase的ATP水解活性降低。ANM标记Ca2+-ATPase磷酸化微区的r(t)曲线半衰期减至68±4nsec。结果提示,膜脂中氧化磷脂的含量影响膜脂双层的流动性及Ca2+-ATPase的ATP水解活性和磷酸化微区的微细结构。  相似文献   

11.
The membrane activity of Na+, K(+)-ATPase, Mg2+, Ca(2+)-ATPase, mitochondrial NAD-isocitrate dehydrogenase, mitochondrial and cytosolic L-glycerol-3-phosphate dehydrogenase was determined in the liver and brain of Wistar rats under acute hypoxic hypoxia against the background of preventive taurine administration. It was shown that preliminary taurine treatment prevented a decrease of hypoxia in activity of Na+. K(+)-ATPase and mitochondrial calcium-dependent enzymes, mostly in the liver. Changes in the intracellular calcium content and biomembrane structure have been discussed as the mechanisms of the taurine effect on the enzymes' activity.  相似文献   

12.
将大鼠置于不同模拟海拔高度低压舱内4d,观察其左、右心室功能代偿与失代偿的某些生物化学基础。结果表明,5000m中度缺氧4d使左、右心室功能、重量、心肌蛋白含量及Ca~(2 )-ATP酶活性均有不同程度的增高。提示机体在整体、心脏器官及心肌细胞分子各个水平的代偿机制均有加强。8000m重度缺氧4d后,左室重量增加,dp/dt_(max)与蛋白含量均下降,肌原纤维ATP酶活性则保持中度缺氧的代偿水平,提示左心功能似已受到损害。与此同时,右室蛋白含量虽也明显减少,但其ATP酶活性则继续增高,dp/dt_(max)未出现下降,表明右心功能仍具有相当的代偿能力。从而支持我们关于在短期内因供氧严重不足而造成的左室心肌的直接损伤作用大于右室心肌的推论。  相似文献   

13.
The amelioration of cardioprotective effect of estrogen in diabetes suggests potential interactive action of estrogen and insulin on myofilament activation. We compared Ca2+-dependent Mg2+-ATPase activity of isolated myofibrillar preparations from hearts of sham and 10-wk ovariectomized rats with or without simultaneous 8 wk-induction of diabetes and from diabetic-ovariectomized rats with estrogen and/or insulin supplementation. Similar magnitude of suppressed maximum myofibrillar ATPase activity was demonstrated in ovariectomized, diabetic, and diabetic-ovariectomized rat hearts. Such suppressed activity and the relative suppression in alpha-myosin heavy chain level in ovariectomy combined with diabetes could be completely restored by estrogen and insulin supplementation. Conversely, the myofilament Ca2+ hypersensitivity detected only in the ovariectomized but not diabetic group was also observed in diabetic-ovariectomized rats, which was restored upon estrogen supplementation. Binding kinetics of beta1-adrenergic receptors and immunoblots of beta1-adrenoceptors as well as heat shock 72 (HSP72) were analyzed to determine the association of changes in receptors and HSP72 to that of the myofilament response to Ca2+. The amount of beta1-adrenoceptors significantly increased concomitant with Ca2+ hypersensitivity of the myofilament, without differences in the receptor binding affinity among the groups. In contrast, changes in HSP72 paralleled that of maximum myofibrillar ATPase activity. These results indicate that hypersensitivity of cardiac myofilament to Ca2+ is specifically induced in ovariectomized rats even under diabetes complication and that alterations in the expression of beta1-adrenoceptors may, in part, play a mechanistic role underlying the cardioprotective effects of estrogen that act together with Ca2+ hypersensitivity of the myofilament in determining the gender difference in cardiac activation.  相似文献   

14.
The activity of Na+/K+- and Ca2+-ATPase and some allosteric properties of Na+/K+-ATPase were studied in whole erythrocytes and their membrane preparations (ghosts) from rats exposed to intermittent altitude hypoxia (10 and 24 exposures, 8 h/day in an altitude chamber, stepwise up to an altitude of 7,000 m). Ca2+-ATPase activity was increased both in whole erythrocytes and ghosts after the first phase of acclimatization (10 exposures). In a standard incubation medium (containing 3 mmol.l-1 MgCl2 ), Na+/K+-ATPase activity in the ghosts was also increased after the initial phase of acclimatization whereas in whole erythrocytes Na+/K+-ATPase was only decreased in the regression phase. At high MgCl2 concentrations (12 mmol.l-1) changes of Na+/K+-ATPase activity both in whole erythrocytes and in the ghosts followed similar time course with a pronounced increase in the first phase of acclimatization (10 exposures) followed by an abrupt drop (24 exposures) and then by a gradual normalization in the regression phase. Sensitivity of the enzyme to mounting MgCl2 concentrations was increased in the ghosts at the end of acclimatization and was decreased in whole erythrocytes during acclimatization and especially in the regression phase. It has been suggested that chronic altitude hypoxia leads to the alteration of cooperative interaction of the Na+/K+-ATPase subunits in the erythrocyte membrane and accumulation of some factor in the cells inhibiting this enzyme.  相似文献   

15.
The superoxide radicals generated by the xanthine oxidase reaction reduced the myofibrillar Ca2+-ATPase activity. This negative effect was prevented by superoxide dismutase or by dithiothreitol, a protective thiol compound. Partial protection was achieved by catalase, while mannitol was ineffective. The myofibrillar Ca2+-ATPase exposed to O2-. radicals did not modify the affinity for Ca2+ while it showed a remarkable reduction of Vmax measured at the saturating level of Ca2+. The O2-. inhibited myofibrillar ATPase showed a higher value of Km for the cofactor associated to a reduced value of Vmax when studied in the presence of increasing concentration of ATP. Thus, circumstances that enhance the production of cardiac O2- radicals can be considered a negative metabolic event capable of depressing the myofibrillar Ca2+-ATPase activity.  相似文献   

16.
Functional properties of myofibrils from chronically ischemic canine myocardium were evaluated. Ischemia was produced by tight stenosis of left anterior descending artery (LAD), followed by 40 min acute ischemia with prior preconditioning. Animals of the first group were sacrificed after 8 weeks. In the second group, angioplasty of LAD was performed after 8 weeks of ischemia and animals were kept alive for other 4 weeks. Control animals were sham operated. Activity and kinetic parameters of myofibrillar Ca2+-stimulated Mg2+-ATPase were measured in myofibrils isolated from anterior and posterior parts of all hearts. We did not find any differences in maximal velocity (Vmax), half-maximal activation constant for calcium (K(Ca2+)50) and cooperativity coefficient (n(hill)) of myofibrils from different experimental groups as compared to controls, either at pH 7, pH 6.5 (acidosis) or pH 7.5 (alkalosis). K(Ca2+)50 increased in medium simulated acidosis (12.6-33.5 times) and n(hill) decreased significantly in all groups as compared with values obtained at pH 7. These results indicate that activity and Ca2+-sensitivity of myofibrillar Mg2+-ATPase remain unchanged despite deteriorated heart function 8 weeks after LAD obstruction. Experiments have confirmed that Ca2+-stimulated-ATPase from canine heart myofibrils responded to pH decrease by a decreased sensitivity to Ca2+ and a decreased cooperativity. However, sensitivity of the enzyme to the pH changes is unaltered by 8 weeks of chronic ischemia.  相似文献   

17.
Tang B  Tang M  Du YM  Liu CJ  Hong ZG  Luo HY  Hu XW  Song YL  Xi JY  Hescheler J 《生理学报》2004,56(5):625-631
为了从离子通道水平上探讨机体低氧适应的离子机制,本实验将雄性 SD 大鼠随机分为常氧对照组和慢性间歇性低氧组[氧浓度(10 ± 0.5) %, 间断缺氧每天 8 h]。用酶解法急性分离单个大鼠肺内动脉平滑肌细胞(pulmonary artery smoothmuscle cells, PASMCs),以全细胞膜片钳技术记录 PASMCs 膜上的电压门控性钾通道 (voltage-gated potassium channel, KV) 电流,观察急性缺氧对慢性间歇性低氧大鼠 PASMCs 的 KV 的影响, 为机体适应低氧能力提供实验依据。结果显示:⑴常氧对照组在电流钳下,急性缺氧可使膜电位明显去极化(由-47.2 ±2.6 mV 去极到 -26.7 ±1.2 mV ); 在电压钳下, 急性缺氧可显著抑制 KV电流( 60 mV 时, KV电流密度从 153.4 ± 9.5 pA/pF降到 70.1 ± 10.6 pA/pF), 峰电流的抑制率为(57.6 ± 3.3) %, 电流-电压关系曲线向右下移。⑵慢性间歇性低氧组KV电流密度随低氧时间延长而逐渐减少(慢性低氧10 d后就有显著性意义),电流- 电压关系曲线逐渐右下移。⑶急性缺氧对慢性间歇性低氧大鼠PASMCs KV电流的抑制作用随慢性间歇性低氧时间延长而逐渐减弱。上述观察结果提示慢性间歇性低氧减弱急性缺氧对 KV 的抑制, 这可能是机体低氧适应的一种重要机制。  相似文献   

18.
19.
The effect of cholesterol incorporation and depletion of the cardiac sarcolemmal sacs on (Ca2+ + Mg2+)-ATPase activity was examined. Cholesterol incorporation to the sarcolemmal sacs was achieved utilizing an in vivo and an in vitro procedure. Cholesterol depleted membranes were obtained in vitro after incubation of the sarcolemmal sacs with inactivated plasma. Arrhenius plots of the (Ca2+ + Mg2+)-ATPase activity showed a triphasic curve when the assays were carried out using a temperature range between 0 and 40 degrees C. The sarcolemmal (Ca2+ + Mg2+)-ATPase activity was shown to be inversely proportional to the cholesterol concentration of the membranes, showing a low ATPase activity with a high cholesterol content and a high ATPase activity when the cholesterol concentration was low. Although the (Ca2+ + Mg2+)-ATPase activity was found to be inhibited in the cholesterol incorporated sarcolemmal sacs, the withdrawal of small amounts of cholesterol from the membranes produced an important stimulatory effect. Changes in (Ca2+ + Mg2+)-ATPase activity due to variation in the membrane cholesterol concentration were shown to be reversible. Our results indicate the possibility of a slow exchange of cholesterol between the tightly bound lipid surrounding the (Ca2+ + Mg2+)-ATPase and the bulk lipid of the sarcolemma.  相似文献   

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