Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While laboratory experimental model of coronary heart disease (according to Frol'kis et al.) is developed, activity of succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, Na+, Ka(+)- and Mg2+ ATPase decreases, but activity of lactate dehydrogenase and concentrations of lactic and pyruvic acids in the heart tissue increase. At the same time concentration of glycogene increases more than twice. As far as we can see there is an evidence of a decrease of glycogene utilization due to change in levels of regulatory processes. Despite a decrease of ATP synthesis by the inhibition of tricarboxylic acid cycle the ATP:ADP relation reduces to ATP, as emphatic inhibition of ATPase in the heart tissues takes place in development of the model of the coronary heart disease. The relation between ATP and ADP is considered as a regulator of glycogene utilization. In the liver tissue activity of succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, Na+, K(+)- and Mg2+ ATPase falls, while concentrations of lactic acid grow. No accumulation of glycogen is observed. It is obvious that there are controversial metabolic processes. Experimental data are discussed.
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PMID:[The relation between oxidative processes and the glycogen content in the heart and liver of rabbits with chronic ischemic heart disease]. 148 3

The inhibitor calmodulin (R 24571) was examined for effects on the activity of red blood cell Ca-ATPases in patients with coronary heart disease during the treatment with nitrates, beta-blockers and calcium antagonists. The maximum activity of Ca-ATPase was measured in the erythrocytes perforated with saponine in the presence of endogenous regulators at a concentration of Ca2+ of 3-5 microM. Patients with high and low Ca-ATPase activity were identified. In the control group R24571 failed to affect Ca-ATPase activity. In patients, the calmodulin inhibitor caused both Ca-ATPase activation and inhibition. The effects of R 24571 correlated with the severity of the patients' condition. In effective therapy, the action of the calmodulin inhibitor became lower on Ca-ATPase activity. It was concluded that there was Ca-ATPase regulation imbalance in patients with coronary heart diseases.
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PMID:[Study of the calmodulin-dependent regulation of calcium adenosine triphosphatase of erythrocyte membranes in patients with ischemic heart disease]. 183 26

Epidemiologic studies have shown that insulin is a risk factor for coronary heart disease (CHD). Clinical studies have also demonstrated positive correlations between insulin and blood pressure, triglycerides, total cholesterol, fibrinogen, and plasminogen activator inhibitor. Moreover, there is an inverse correlation between insulin and high-density lipoprotein (HDL). These studies have provided evidence in support of the biologic plausibility of epidemiologic observations, but they have not clearly established insulin's role in the pathogenesis of human cardiovascular diseases (CVD) such as hypertension. In fact, there is considerable evidence that insulin resistance (abnormal nonoxidative glucose disposal), not hyperinsulinemia, is the primary insulin-related abnormality in human hypertension, and that hyperinsulinemia occurs as a response to insulin resistance. Skeletal muscle appears to be the primary site of insulin resistance in essential hypertension, although other organs, such as the kidneys and liver--key sites for cell and water homeostasis and lipoprotein regulation, respectively--may respond normally to insulin. Adipocytes also appear to be a site of insulin resistance. Thus, the putative interrelationship between hyperinsulinemia and insulin resistance, on the one hand, and with blood pressure and lipoproteins, on the other, is a complex one and may involve organ-specific insulin resistance. Altered cation transport is one of several mechanisms by which insulin resistance might raise blood pressure. The Na+, K(+)-ATPase and Ca(2+)-ATPase pumps are insulin sensitive. Thus, when insulin resistance is present, the activity of these pumps in the smooth muscle of the arterial wall might be reduced. This would lead to an intracellular accumulation of sodium and calcium, thereby sensitizing the vascular wall to pressor substances. Moreover, secondary hyperinsulinemia will occur, and insulin has been shown to stimulate sympathetic nervous system activity and to increase renal tubular absorption of sodium. Insulin is also a growth factor and therefore might have a trophic effect on the vessel wall, one that could initiate and/or sustain hypertension as well as atherosclerosis. Abnormal lipoprotein metabolism is yet another possible explanation for the accelerated atherosclerosis that has been observed in persons with abnormal carbohydrate tolerance and insulin resistance. Hyperinsulinemia and insulin resistance both play a role in the expression of elevated very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) levels as well as in the depression of HDL levels. Coronary risk reduction has been disappointing when blood pressure has been lowered with treatment regimens based on thiazide diuretics and/or beta blockers. Thiazides and some beta blockers may further impair tissue insulin sensitivity and often cause blood lipoprotein abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiologic and clinical aspects of insulin resistance and hyperinsulinemia. 186 24

The purpose of the present work was to evaluate the clinical efficacy and the mechanism of Yi-qi Huo-xue Injection (YHI) in treatment of coronary heart disease. YHI consists of Ginseng, Astragalus and Angelicae Sinensis. The 10% dextrose serves as a placebo. The results were as follows: 1. the frequency and severity of angina episodes were reduced by 90.63%; 2. the ischemic ST-T in ECG was improved in 56.25% of cases; 3. the tolerance to treadmill exercise was increased from 348.50 to 503.50 M.; 4. the left ventricular function was strengthened, PEP/LVET ratio reduced from 0.45 to 0.36, the activity of (Na(+)-K+) ATPase in myocardial cell membrane of rats inhibited by 19.2%; 5. the blood viscosity and erythrocyte electrophoretic time lowered; 6. the adhesion and aggregation of platelet in patients with CHD were inhibited by 27% and 59.4% respectively; 7. the plasma TXB2 level in CHD was reduced from 260.28 +/- 164.4 to 139.29 +/- 57.01 pg/ml; 8. the plasma 6-keto-PGF1 alpha level in CHD was increased from 33.45 +/- 22.5 to 57.48 +/- 13.1 pg/ml, and in rats from 185.77 to 366.33 pg/ml. The differences were all statistically significant (P less than 0.05-0.01) in comparison with the placebo group.
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PMID:Clinical and experimental studies of coronary heart disease treated with yi-qi huo-xue injection. 261 56

Functional disorders in the ion-transport ATPase system were detected in young and middle-aged males suffering from coronary heart disease (CHD). The degree of the ATPase activity impairment (general ATPase, Mg-ATPase and Na, K-ATPase) correlated with hyperlipoproteinemia (HLP) which was revealed in CHD patients. Different direction of changes was observed in the concentrations of cations in plasma and erythrocytes, that, in some cases, could not be correlated with the degree of HLP and suppression of ion-transport ATPase activity. Positive correlation was observed with respect to increased concentration of Mg2+ in serum and Na+ in erythrocytes, and hypercholesterolemia, as well as with respect to decreased concentration of Mg2+, suppressed Mg-ATPase activity, and hypo-alpha-cholesterolemia. A significant tendency to normalization of parameters of lipid metabolism and lipid-dependent ion-transport ATPases was recorded in CHD patients after a course of the anti-atherosclerotic dietotherapy.
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PMID:[The effect of the alimentary factor on erythrocyte ATPase activity in ischemic heart disease patients]. 282 Jan 51

Structural characteristics and Na, K-ATPase activity of erythrocyte membranes were studied by the spin probe method in patients with an angiographically verified damage to the coronary arteries. The rise of the cholesterol/phospholipid ratio in patients with coronary heart disease was associated with the increased orderliness of the fatty acid chains of erythrocyte membrane lipids, leading to inhibition of Na, K-ATPase activity. The data point to the same line of changes in erythrocyte membranes and smooth muscle cells during the development of coronary heart disease.
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PMID:[Changes in the structural characteristics and ATPase activity of the erythrocyte membranes in angiographically verified coronary artery lesion]. 608 59

In acutely uremic animals, the contractile force of the heart is consistently increased; such an increase can be dissociated from changes of afterload or catecholaminergic drive. It is associated with diminished sarcolemmal Na,K-ATPase activity in the heart which, in turn, may be related to increased levels of endogenous digitalis-like substances (endigens) that have been postulated to represent a natriuretic factor. In patients with chronic uremia, myocardial contractility is usually normal, but occasionally there may be heart failure unrelated to pre-existing hypertension, coronary heart disease, anemia, fluid overload, or other recognizable factors. So far, the experimental basis for this clinical observation is uncertain. Possible causes for the clinical syndrome include an excess of parathyroid hormone or cardiodepressor substances. There is experimental evidence of impaired cardiac response to beta adrenergic agonists, e.g., decreased isoproterenol-dependent calcium uptake, diminished inotropic and chronotropic responses. In acutely uremic rats, cardiac cyclic AMP levels are high but can be reversed by beta blockers. Heart calcium content is variable and heart weight is constantly increased in acutely uremic rats, despite decreased skeletal muscle mass. The change in heart weight is not related to anemia, to an excess of parathyroid hormone, or to sympathetic activity; its cause remains unknown. Experimental studies to date have shown a variety of abnormalities, but do not provide a uniform concept of the mechanisms or an explanation for the cardiac dysfunction so often observed in patients with uremia.
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PMID:Cardiac function in experimental uremia. 636 51

In 743 cases, the TCM and WM susceptible factors of senile cataract (SC) was studied by the clinical epidemiological investigation. By single factor analysis, the result showed that in WM, the susceptible factors of SC mostly related to (1) case history: coronary heart disease, old ages, smoking, multiple offsprings; (2) physical sign: short build, with coronary sulcus, higher systolic pressure, pulse pressure and average arterial pressure; (3) cardiovascular function: abnormal EKG, higher heart beat index, short microcirculatory stasis time, lower carrier viscosity of blood; (4) dysfunction of brain; (5) deficiency of pulmonary function; (6) lower RBC ATPase, higher whole blood reduction viscosity. While in TCM, it was related to (1) old aged and general asthenia, (2) deficiency of Qi, Heart, Liver or Kidney, (3) Blood Stasis. By stepwise regression analysis, the result showed that SC occurred through the combination with 13 factors of TCM and WM, including Yin Deficiency, senility index, hemorheology index, brain function, pulmonary function, blood pressure, body height, character, optical fundus, etc.
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PMID:[Investigation on traditional Chinese medicine and Western medicine susceptible factors on senile cataract]. 795 Feb 14

Fasting plasma triglyceride (TG), total cholesterol(TC), low density lipoprotein-cholesterol(LDL-C), high density lipoprotein-cholesterol(HDL-C), activities of erythrocyte membrane Na(+)-K(+)-ATPase, Ca(2+)-ATPase, Mg(2+)-ATPase, and intraerythrocytic calcium concentration were examined in 21 patients with coronary heart disease(CHD) and 21 normal controls. It was found that the plasma contents of TG, TC, LDL-C and intraerythrocytic [Ca2+] in patients with CHD were much higher while plasma contents of HDL-C, activities of erythrocyte membrane Na(+)-K(+)- and Ca(2+)-ATPase were much lower than those of normal controls. Mg(2+)-ATPase activity showed no significant difference between these two groups. The activities of erythrocyte membrane Na(+)-K(+)- and Ca(2+)-ATPase were negatively correlated with plasma TG, TC, LDL-C levels, respectively, and positively correlated with plasma HDL-C. The possible pathogenic mechanism is discussed on the basis of our results.
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PMID:[Changes of erythrocyte membrane ATPase activities and plasma lipids in patients with coronary heart disease]. 1193 46

Physical inactivity is an independent risk factor for coronary heart disease, yet the mechanism(s) of exercise-related cardioprotection remains unknown. We tested the hypothesis that coronary smooth muscle after exercise training would have decreased mitogen-induced phenotypic modulation and enhanced regulation of nuclear Ca(2+). Yucatan swine were endurance exercise trained (EX) on a treadmill for 16-20 wk. EX reduced endothelin-1-induced DNA content by 40% compared with sedentary (SED) swine (P < 0.01). EX decreased single cell peak endothelin-1-induced cytosolic Ca(2+) responses compared with SED by 16% and peak nuclear Ca(2+) responses by 33% (P < 0.05), as determined by confocal microscopy. On the basis of these results, we hypothesized that sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and intracellular Ca(2+) stores in native smooth muscle are spatially localized to dissociate cytosolic Ca(2+) and nuclear Ca(2+). Subcellular localization of SERCA in living and fixed cells revealed a distribution of SERCA near the sarcolemma and on the nuclear envelope. These results show that EX enhances nuclear Ca(2+) regulation, possibly via SERCA, which may be one mechanism by which coronary smooth muscle cells from EX are less responsive to mitogen-induced phenotypic modulation.
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PMID:Exercise training attenuates coronary smooth muscle phenotypic modulation and nuclear Ca2+ signaling. 1238 2


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