复合离子盐对老年人血压、血脂、血糖及胰岛素的影响

目的：探讨在不减少盐摄入总量的前提下，复合离子盐对老年人血压、血脂、血糖及胰岛素的影响。方法：在社区中抽取226例老年人作为研究对象，其中高血压患者112例，正常血压者114例。两组再随机分为离子盐组和加碘盐组．分别给予摄入复合离子盐和普通加碘盐，6个月后观察其血压、血脂、血糖及血浆胰岛素水平的变化。结果：高血压患者中．复合离子盐组较普通加碘盐组血压明显下降（P〈0．01），复合离子盐对正常血压影响较小，但可以延缓血压升高（P〈0．01）。两组血脂、血糖及血浆胰岛素水平没有显著差异。结论：复合离子盐可以降低血压，对血脂、血糖和血浆胰岛素水平无明显影响。     

原发性高血压肾病患者红细胞ATP酶活性检测的临床意义

目的 探讨原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶活性的改变参与原发性高血压肾病的可能机制。方法 按Reilni制膜法测定32例原发性高血压无肾病和40例原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶含量,并与35名正常健康人作比较。结果 原发性高血压无肾病组和肾病组细胞膜Na^＋、K＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶活性均显著地低于正常人组（P〈0.01）。原发性高血压肾病组与无肾病组亦有显著性差异（P〈0.05）。结论 原发性高血压肾病的发生和发展与细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP的活性有密切的关系。     

利多卡因对家兔心肌缺血/再灌注损伤氧自由基及Na+-K+-ATPase、Ca2+-Mg2-ATPase的作用

目的观察利多卡因对心肌缺血再灌注损伤家兔血清GSH—P^2X、MDA及心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase的影响。方法24只家兔随机分为3组：假手术组（A组）、缺血／再灌注组（B组）、利多卡因组（c组）,每组8只。B组、C组阻断左冠状动脉前降支40min．再灌注90min．A组仅穿线不结扎。C组于开放冠状动脉再灌注前经颈静脉注射利多卡因5mg／kg,B、C组注射等量生理盐水。于再灌注90min取颈静脉血测定GSH—PX、MDA;再灌注90min后取心肌组织测定Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase。结果血清GSH—PXB组较A、C组降低（P〈0．01）、血清MDAB组较A、C组升高;心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase B组较A、C组降低（P〈0．01）。结论利多卡因对心肌缺血再灌注损伤具有保护作用。     

窒息新生儿血电解质动态变化分析

目的分析窒息新生儿血清电解质动态变化及意义。方法窒息组新生儿343例按窒息程度分为轻度窒息组297例,重度窒息组46例;另设对照组41例。采用酶法测定血清K^＋、Na^＋、Cl^-、Ca^2＋浓度。结果窒息组新生儿血清K^＋、Cl^-、Ca^2＋水平显著低于对照组（均P〈0．01）;出生后24～48h血清K^＋、Na^＋、Cl^-、Ca^2＋水平显著低于24h内（均P〈0．01）;生后24—48h低钠血症、低氯血症、低钙血症的发生率显著高于24h（均P〈0．01）。轻、重度窒息组K^＋、Na^＋、Cl^-、Ca^2＋水平差异无统计学意义（均P〉0．05）。结论新生儿窒息后48h内血清K^＋、Na^＋、Cl^-、Ca^2＋水平逐渐降低,电解质紊乱发生率逐渐增高,应常规动态监测血电解质变化以指导及时治疗。     

线粒体及内质网对铅引起的[Ca2+]i升高的作用

目的 研究线粒体、内质网Ca^2 -ATP酶以及Na^ 和K^ -ATP酶活力的改变对铅引起的[Ca^2 ]i升高的调节作用，探讨铅引起的[Ca^2 ]i增高对学习记忆功能的影响。方法 Wistar大鼠神经肉瘤C6细胞培养于含醋酸铅的培养液中，于不同时间终止染铅，检测[ca2’]；及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力。结果 (1)0．2μmol／L染铅组：[Ca^2 ]i轻度升高，线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力升高，内质网酶活力略增高；(2)1．0μmol／L染铅组：[Ca^2 ]；于染铅后0．5h升至最高，以后逐渐降低，波动于iL60～190nmol／L之间；线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶于染铅后0．5h升至最高(分别为未染铅前酶活力的29．1、39．2、10．8和19．8倍)，2d后降至接近正常水平。结论 (1)铅可使Wistar大鼠神经肉瘤C6细胞Ca^2 浓度及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高；(2)当[Ca^2 ]i增高不显著时以线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高为主；当[Ca^2 ]i急剧升高时，线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力均明显增高，尤其是线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高更为显著。     

青龙衣多糖对H22型肿瘤细胞的ATPase活性影响的研究

目的 研究青龙衣多糖对H22型肿瘤细胞的ATPase活性的影响。方法 按照测定无机磷含量的方法对H22肿瘤细胞的Ca^2＋-ATPase、Na^＋K^＋-ATPase和Mg^2＋-ATPase活性进行了测定。结果 发现青龙衣多糖可以降低ATPase的活性，除青龙衣多糖中、高剂量组显著抑制Ca^2＋-ATPase活性。高、中、低剂量组都显著降低Na^＋-K^＋-ATPase和Mg^2＋-ATPase活性（P〈0．05）。结论 ATPase活性降低导致了膜电位下降。细胞容积降低．可能引起细胞凋亡发生．Ca^2＋．调节凋亡发生．Mg^2＋调控ATPase的活性,可能是青龙衣多糖抗肿瘤的机制之一。     

肥胖儿童高血压发病因素有机理的研究

目的：探讨儿童肥胖引起高血压的机制。方法：测定104例12－16岁儿童的血脂、胰岛素水平,Na^ -K^ -ATP酶和Ca^2 -ATP酶活性。结果：在正常血压肥胖组（ONT）和高血压肥胖组（OHT）,空腹胰岛素（Ins）显著升高,面NNa^ -K^ -ATP酶和Ca^2 -ATP酶活性显著下降,三者在ONT和OHT组之间也有显著性差异,在OHT组Ins升高,两酶活性下降,Pearson相关和多元回归分析显示,在OHT组,Ins和Ca^2 -ATP酶与收缩压（SBP）显著相关,Na^ -K^ -ATP酶与舒张压9DBP）显著相关。结论：高胰岛素血症、Na^ -K^ -ATP酶和Ca^2 -ATP酶活性降低可能在肥胖儿童高血压的发病机制中起重要作用。     

安氟醚麻醉下牵拉胆囊对心肌ATP酶、ET、NOS的影响

目的 研究安氟醚麻醉下牵拉胆囊对心肌ATP酶、ET、NOS的影响。方法 健康家兔24只，随机分为A、B、C三组，A组对照组，B组吸入安氟醚达0．65MAC，C组吸入安氟醚达1．3MAC。暴露胆囊，坠以100g重物牵引10分钟。迅速开胸，取心肌组织测定ATP酶、内皮素(ET)、一氟化氯合成酶(NOS)。结果 三组心肌细胞的Na^2 —K^ ATPase、Mg^2 -ATPase差异元显著性，C组的Ca^2 -ATPase明显低于A组(P＜0．05)，B组、C组的ET明显低于A组(P＜0．05)。结论 安氟醚麻醉下牵拉胆囊可抑制了心肌细胞Ca^2 -ATPase和ET的释放。     

复合离子盐对自发性高血压大鼠胰岛素抵抗相关因素的影响

目的 :本研究通过观察不同剂量复合离子盐对自发性高血压大鼠 (SHR)胰岛素抵抗相关因素的影响 ,探讨复合离子盐能否对原发性高血压起到防治作用。方法 :对61只自发性高血压大鼠分别饲以复合离子盐 (高、低盐实验组 )及普通加碘盐 (高、低盐对照组 ) ,动态观测动物血压变化 ,检测大鼠血糖、血胰岛素水平,计算胰岛素敏感指数。结果 :(1)复合离子盐较普通加碘盐具有明显的预防高血压作用 ,高盐实验组血压明显低于高盐对照组(P<0.01)。 (2)4组血糖水平差别无统计学意义 (P>0.05) ;高盐对照组胰岛素水平高于其他3组 (P<0.05) ,胰岛素敏感指数明显低于其他3组 (P<0.05)。高盐实验组血糖和胰岛素水平与低盐实验组差别无统计学意义 (P>0.05)。结论 :复合离子盐对SHR的高血压有防治作用 ,且不增加胰岛素抵抗     

脑健冲剂对AD大鼠线粒体结构及离子泵ATP酶的影响

目的 观察脑健冲剂对加大鼠线粒体结构及离子泵ATP酶的影响。方法 采用D-半乳糖致衰老基础上β—淀粉样蛋白颅内注射所致AD大鼠模型。将Wista大鼠随机分为6组：空白组、假损伤组、模型组、对照组、治疗组、保护组，通过电镜观察及比色法，观察脑健冲剂的作用。结果 脑健冲剂能使AD大鼠的Ca^ —ATP酶、Ca^2 Mg^2 —ATP酶、Na^ K^ —ATP酶活力水平明显提高。用药组的线粒体体密度、面数密度和平均截面积与模型组相比差异有非常显著意义(P＜0．01)。结论 脑健冲剂能改善AD大鼠的线粒体损伤程度，提高加大鼠的线粒体离子泵ATP酶的活力。     

前胡香豆素对肾型高血压大鼠左室肥厚及心肌胞内钙、Na+,K+-ATP酶和Ca2+,Mg2+-ATP酶活性的影响

目的研究前胡香豆素组分对肾型高血压左室肥厚的预防和逆转作用及机制。方法用两肾一夹肾型高血压左室肥厚大鼠(RHR)模型,测定前胡香豆素组分对其血压、左室湿重、心肌细胞面积、胞内静息钙及胞膜和线粒体ATP酶活性的影响。结果前胡香豆素组分(30 mg·kg^-1·d^-1,ig)预防组及逆转组大鼠血压、左室湿重/体重均较肥厚组明显降低;左室心肌细胞面积、胞内静息钙均较肥厚组降低;对KCl致钙浓度升高亦明显低于肥厚组;两组均可增加心肌细胞膜及线粒体Na⁺,K⁺-ATP酶和Ca²⁺,Mg²⁺-ATP酶活性。结论前胡香豆素组分可预防及逆转RHR左室肥厚,减少心肌细胞内钙含量,增加ATP酶活性。     

2型糖尿病患者血中升压因子作用机制的探讨

目的：了解２型糖尿病患者（ＮＩＤＤＭ）血中升压因子水平及相关离子转运酶的变化,探讨对血压相互影响的机制。方法：采用生我省在性测定方法测定了３２例２型糖尿病患者和３３例健康人血中升压因子活性,用化学法测定Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶、Ｃａ＾２＋－Ｍｇ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶活性变化。结果：糖尿病组和正常组升压因子阳性纺有显著性差异;糖尿病组的升压模式与自发性高血压大鼠（ＳＨＲ）的有所不同;ＮＩＤＤ     

Effects of calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes

1. The effects of 11 calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes were studied. 2. All the calcium antagonists studied had inhibitory effects on ouabain-sensitive (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities in synaptosomes at high concentrations (10 or 100 microM). 3. Calcium antagonists such as trifluoperazine, flunarizine and cinnarizine had inhibitory effects on Ca2+-ATPase activity at low concentrations (1-10 microM). 4. Trifluoperazine and La3+ had inhibitory effects on Mg2+-ATPase activity at low concentration (1 microM). 5. Our results suggest that most of the calcium antagonists studied have little effects on neuronal (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities at therapeutic dose ranges (1 microM or lower).     

Stimulation of neuronal Na+, K+-ATPase by calcium

The effect of calcium on ATP-phosphohydrolase activity of rat brain homogenates has been investigated. In both the presence and absence of the chelating agent EDTA, free calcium within the concentration range 1.2 x 10(-7) to 5.0 x 10(-4) moles/l consistently affected only the activity of Na+, K+-ATpase; the activities of Mg2+-ATPase and Na+-ATPase were essentially unchanged by Ca2+; Ca2+-ATPase could not be demonstrated. In either the presence or absence of EDTA, concentrations of free-Ca2+ above 3 x 10(-6) moles/l caused an inhibition of Na+,K+-ATPase activity. In the presence of EDTA, concentrations of free-Ca2+ below 3 x 10(-6) moles/l were ineffective at altering Na+, K+-ATPase activity but, in the absence of EDTA, free-Ca2+ in this concentration range caused a marked stimulation of the enzyme. Evidence is presented to show that the stimulation of Na+, K+-ATPase by calcium is modulated by the regulatory protein calmodulin. Since the stimulation occurs over the range of concentrations at which calcium would be expected to be encountered within the cell, it is suggested that this is the major physiological effect of calcium on Na+, K+-ATPase.     

利多卡因对家兔心肌缺血／再灌注损伤Na^＋-K^＋-ATPase、Ca^2＋ -Mg^2＋ -ATPase及NO的作用

目的:研究利多卡因对心肌缺血/再灌注损伤家兔心肌Na -K -ATPase、Ca2 -Mg2 -ATPase及血清NO的影响。方法:24只家兔随机分为3组:假手术组(A组)、缺血/再灌注组(B组)、利多卡因组(C组),每组8只。B组、C组阻断左冠状动脉前降支40 min,再灌注90 min,A组仅穿线不结扎。C组于开放冠状动脉再灌注前经颈静脉注射利多卡因5 mg/kg,A、B组注射等量生理盐水。于再灌注90min取颈静脉血测定NO。再灌注90 min后取心肌组织测定NOS、Na -K -ATPase、Ca2 -Mg2 -ATPase。结果:心肌组织Ca2 -Mg2 -ATPaseB组较A、C组降低(P<0.01);Na -K -ATPase B组较A、C组降低(P<0.01);血清NO、心肌组织NOS:B组较A、C组降低(P<0.01)。结论:利多卡因对心肌缺血/再灌注损伤具有保护作用。     

Palytoxin acts through Na+,K+-ATPase

Palytoxin is the most potent animal toxin, with a unique structure. The author's group has searched for its mode of action with the following results: 1. Palytoxin (1 pM and less) causes a fast K+ outflow from erythrocytes; 2. Extracellular Ca2+ and borate, and intracellular ATP enhance, but ouabain potently inhibits the palytoxin effects; 3. Palytoxin increases the permeability for Na+ and K+ but not for Ca2+; 4. Palytoxin in comparatively high concentrations (100 nM and above) inhibits Na+,K+-ATPase; 5. Palytoxin can be radiolabeled with 125I. Its receptor is very similar to, but not identical to that of ouabain. A reaction scheme has been delineated which allows an explanation to be obtained for all the known actions of palytoxin. It centers on the hypothesis that palytoxin binds to Na+,K+-ATPase and converts the enzyme or its close vicinity into an open channel with the permselectivity measured on erythrocytes. Patch clamp data from myocytes were obtained in other laboratories. They prove the presence of the predicted palytoxin channel.     

Cholinergic regulation of Na+-K+-ATPase activity in rat parotid gland: changes after castration

In this study, we investigated the different signalling pathways involved in muscarinic acetylcholine M(3) receptor-dependent modulation of Na(+)-K(+)-ATPase in parotid glands from normal and castrated rats. Carbachol inhibited the enzyme activity in parotid glands from control rats while it stimulated the enzyme activity in castrated rats. The inhibition of Ca(2+) calmodulin by trifluoperazine abolished the inhibitory effect of carbachol in control rats, while the inhibition of protein kinase C by staurosporine stimulated Na(+)-K(+)-ATPase. In castrated rats, trifluoperazine inhibited the carbachol-stimulant effect while staurosporine had no effect. Results indicate that in control glands the activation of a phospholipid-Ca(2+) calmodulin-dependent protein kinase C is responsible for the inhibitory effect of carbachol on Na(+)-K(+)-ATPase activity. In castrated rats, the activation of the enzyme by carbachol is regulated by its Ca(2+) calmodulin-stimulating action, and not by activation of protein kinase C. The activation of the Na(+)-K(+)-ATPase observed in castrated rats resulted in a decrease in carbachol-induced net K(+) efflux and thereby could decrease salivary fluid production.     

Inhibition of dog kidney Na+, K+-ATPase activity by procaine, tetracaine and dibucaine

The potency of local anesthetics as inhibitors of Na+, K+-ATPase and K+- NPPase activities correlated with lipid solubility. The order of potencies was: dibucaine greater than tetracaine much greater than procaine. Na+-ATPase activity was remarkably more sensitive to inhibition by tetracaine and procaine, and inhibitory potency did not correlate with lipid solubility. The order of potencies for inhibition of Na+-ATPase activity was: tetracaine greater than dibucaine greater than procaine. We examined interactions between the local anesthetics and monovalent cations in an attempt to explain this observation. Inhibition of Na+-K+-ATPase by tetracaine and dibucaine was competitive with respect to Na+, and inhibition of Na+-ATPase activity by all three agents was competitive with respect to Na+. Inhibition of Na+, K+-ATPase activity by procaine and tetracaine was competitive with respect to K+, and inhibition of K+- NPPase activity by all three agents was competitive with respect to K+. Dibucaine, the most lipid soluble agent, was equipotent as an inhibitor of all three activities and was generally less effective as a competitor with respect to activation by monovalent cations. These results suggest that dibucaine may interact nonspecifically with membrane lipids to inhibit enzyme activity whereas less lipid soluble agents, such as tetracaine and procaine, may interact more selectively with cation binding sites. It appears that the presence of K+ in the assay medium specifically decreases the inhibitory potency of tetracaine and procaine. Direct competition between these agents and K+ may prevent inhibition or, alternately, the presence of K+ may convert the enzyme to a conformation less susceptible to inhibition by agents of low to intermediate lipid solubility.     

Mode of inhibitory action of melittin on Na+-K+-ATPase activity of the rat synaptic membrane

The effects of melittin from bee venom, cardiotoxin from Formosan cobra venom, and ouabain on Na+-K+-ATPase activity of the synaptic membrane isolated from rat cerebral cortex were studied. Melittin was the most potent in inhibiting Na+-K+-ATPase activity. Mg2+-ATPase was less susceptible than Na+-K+-ATPase to the inhibitory action of toxins. High K+ (30 mM) reversed the inhibitory action of melittin on Na+-K+-ATPase but did not affect that of cardiotoxin. A comparison between the effects of ouabain and melittin was studied, using double-reciprocal plots of Na+-K+-ATPase activity against K+. It was shown that both were competitive with K+ for binding to the K+ site. Moreover, a median-effect plot revealed that ouabain and melittin antagonized each other when inhibiting Na+-K+-ATPase. Phosphatidylcholine (PC) was the only one of the phospholipids tested capable of protecting Na+-K+-ATPase from the inhibitory action of melittin but not that of ouabain. However, the inhibitory action of cardiotoxin on this enzyme was decreased by phosphatidylserine and sphingomyelin, in addition to PC. All of these findings suggest that the melittin polypeptide potently inhibits Na+-K+-ATPase, possibly by binding to the K+ site.     

Contribution of lipid dynamics on the inhibition of bovine brain synaptosomal Na+-K+-ATPase activity induced by 4-hydroxy-2-nonenal

The effects of lipid hydroperoxide degradation products, such as 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA), on bovine brain synaptosomal ATPase activities and their membrane lipid organization were examined. When the synaptosomes were treated with HNE, this resulted in the decrease of Na(+)-K(+)-ATPase activity with the loss of sulfhydryl (SH) groups in the membrane proteins. In contrast, MDA treatment of the synaptosomes did not induce an appreciable decrease in the ATPase activity or a loss of SH groups. The decreases in ATPase activity and SH content by treatment with HNE were also observed, as a Na+-K+-ATPase preparation was used in place of the synaptosomes. On the other hand, HNE had very little effect on synaptosomal Ca2+- and Mg2+-ATPase activities. The results of the kinetic analysis of the Na+-K+-ATPase activity indicated that the decrease in the activity by HNE-modification is due to a decreased affinity for the substrate. ATP completely protected the ATPase from the HNE attack. Modification of the synaptosomes with HNE caused a decrease in the membrane lipid fluidity near the lipid/water interface, not the lipid layer interior. In addition, it was found that there is a good relationship between the lipid fluidity and the Na+-K+-ATPase activity under the presence of various concentrations of HNE, suggesting that the lipid dynamics are closely related to HNE-induced inhibition of the ATPase activity. On the other hand, MDA did not induce change in the membrane lipid fluidity. HNE and MDA are mainly incorporated into the lipid and protein fractions in the synaptosomal membranes, respectively. Based on these results, we proposed a possible mechanism of HNE-induced inhibition of synaptosomal Na+-K+-ATPase activity associated with alterations in the membrane lipid organization.