Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental model of myocardiopathy was induced in rhesus monkeys following noradrenaline (NA) infusion (20 ug/kg body wt/minute), for a period of 2 hours daily for three consecutive days. The animals were sacrificed after two hours (acute phase), forty-eight hours (sub-acute phase) and twenty-one days (chronic phase). Focal depletion of succinic dehydrogenase, increase in adenosine triphosphatase, acid phosphatase and appearance of large fat droplets in myocardial muscle was noted in the acute phase. Histopathological examination revealed focal edema, opacity and fuchsinorrhagia of the muscle fibres distributed in both the ventricles. Myofibrillar degeneration, myocytolysis and vacuolization with aggregation of lymphomononuclear cells were the significant features in the acute phase. During sub-acute and chronic phases, these features became less prominent and reparative changes with proliferation of fibroblasts became more marked. By the twenty-first day, irregular, focal scars replaced the necrosed myocardium. Ultrastructurally, heart muscle showed myofibrillar disorganisation, distortion of Z and A bands, dilatation of sarcoplasmic reticulum and swelling and rupture of mitochondria. Altered membrane permeability was evidenced by the presence of reaction products of horseradish peroxidase within the cardiac cells. In the reparative phase, however, myocytolytic changes regressed and collagen deposition was the prominent feature. This experimental study has several histological features simulating human cases of myocardial infarction without coronary occlusion.
...
PMID:Catecholamine-induced experimental cardiomyopathy--a histopathological, histochemical and ultrastructural study. 259 40

It has been well documented that acclimatization to chronic high altitude hypoxia involves a complex of adaptation changes which are capable of protecting the myocardium in diverse situations such as in acute hypoxia, coronary occlusion-induced ischaemia or isoprenaline-induced calcium overload. Since many of the former changes concern membrane functions, namely those of the sarcolemma, the activities and kinetic properties of sarcolemmal Mg2+-, Ca2+- and (Na+ + K+)-ATPase were investigated in right heart ventricles of rats acclimatized to intermittent high altitude hypoxia simulated in a barochamber. In the course of the experiment, the ventricles were subjected to a special anoxic test in vitro. The high altitude induced increase in cardiac tolerance to anoxia was not accompanied by any preservation of the sarcolemmal ATPase activities. On the contrary, membrane preparations obtained from the right ventricles of hearts acclimatized to high altitude exhibited significantly lower ATPase activities in comparison to non-acclimatized controls. The significant diminution in Km values of ATPases established in acclimatized hearts points to an increase in the affinity of their active sites to ATP. The latter effect is in agreement with the lowered rate of both the decrease in ATPase activities and the reduction of contractility in acclimatized hearts during the anoxic test, as well as with the considerably improved postanoxic reparability of contractions as compared to the controls. It is being concluded that the sarcolemmal changes at the level of ATPases involved in ionic transport processes represent an integral part of the adaptation complex to chronic high altitude hypoxia.
...
PMID:Increased affinity to substrate in sarcolemmal ATPases from hearts acclimatized to high altitude hypoxia. 282

Global ischemia in guinea-pig hearts for 60 to 90 min depressed microsomal and mitochondrial Ca2+ uptake activities. Reperfusion of the 60 min ischemic hearts resulted in incomplete recovery of contractile function and calcium uptake activities of both mitochondrial and microsomal fractions. On the other hand, reperfusion of the 90 min ischemic hearts further depressed the microsomal Ca2+ uptake activity. Coronary occlusion for 90 min in dog hearts was found to decrease microsomal Ca2+-pump and sarcolemmal Na+-K+ ATPase activities. Reperfusion of these regional ischemic hearts further depressed the microsomal Ca2+ uptake and Ca2+-stimulated ATPase as well as sarcolemmal Na+-K+ ATPase activities whereas mitochondrial Ca2+ uptake was increased. Perfusion of rat hearts for 60 min with hypoxic medium resulted in depression of the sarcolemmal Na+-dependent Ca2+ uptake and ATP-dependent Ca2+ uptake activities. Reperfusion of these hypoxic hearts failed to recover the sarcolemmal Na+-Ca2+ exchange and Ca2+-pump activities. These results demonstrate that membrane defects with respect to Ca2+ transport processes in ischemic/hypoxic hearts may be associated with irreversible injury.
...
PMID:Alterations in heart membrane calcium transport during the development of ischemia-reperfusion injury. 284 10

We investigated the effectiveness of the beta-blocking agent metipranolol in preventing detrimental systemic and myocardial alterations induced in healthy dogs by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Metipranolol (0.3 mg/kg) was infused intravenously concurrently with AD (1.2 micrograms/kg/min) for 4 h and blood values of free fatty acids (FFA) and triiodothyronine(T3) were measured initially, after 2 and 4 h of infusion and compared with those obtained in dogs infused with AD alone and with saline. Metipranolol suppressed a rise in free fatty acid, reversed AD-induced histoenzymatic changes in succinic dehydrogenase and ATPase activity and considerably inhibited the development of mitochondrial alterations detected in dogs infused with AD alone. A tendency to attenuate AD-induced fall in serum T3 was also detected in metipranolol-treated dogs. Results suggest that this drug might be of value in preventing consequences of increased adrenergic activity in the acute stage of myocardial infarction.
...
PMID:Prevention of adrenaline-induced metabolic systemic and myocardial alterations by the beta-blocking agent metipranolol in the dog. 611 91

Effects of myocardial ischaemia on sarcoplasmic reticulum (SR) of dog hearts were investigated. Regional ischaemia was produced by occlusion of the left circumflex artery, and a microsomal fraction enriched in vesicles of SR was isolated from subendocardium (Endo) and subepicardium (Epi) of control and ischaemic areas of the heart. No significant changes occurred in ischaemic Epi. A loss of in vitro activities (ie calcium transport and ATPase) was found for SR from ischaemic Endo which paralleled the changes in the histology of the tissue. At 5 min of coronary occlusion, Ca2+ binding and Ca2+-ATPase activities of SR from ischaemic Endo were normal. A decrease in the activities of SR was first evident at 15 min after the occlusion, decreased further at about 30 min and remained at that level at 60 min of ischaemia. The maximal rate of Ca2+ uptake did not parallel the Ca2+-binding and Ca2+-ATPase activities. The degree of cAMP-dependent phosphorylation by endogenous and exogenous protein kinase was not different between SR from control and ischaemic areas. A participatory role of SR in the ischaemic impairment of left ventricular systolic and diastolic performance is discussed.
...
PMID:Ischaemia-induced changes in canine cardiac sarcoplasmic reticulum. 622 97

The aim of this study was to investigate whether insulin-glucose (IG) is able to prevent detrimental systemic and myocardial changes induced in healthy dog by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Insulin (0.3 u/kg) and glucose (10% ml/kg) mixture was infused intravenously concurrently with AD (1.2 microgram/kg/min) for 4 h and blood values of FFA, triiodothyronine (T3) immunoreactive insulin (IRI) and glucose measured initially, after 2 and 4 h of infusion were compared with the values found in dogs infused with AD alone and with saline. IG suppressed a rise in FFA, attenuated a fall in T3, reversed AD-induced histoenzymatic changes in SDH and ATPase activity and completely prevented the development of mitochondrial alterations shown by electron microscopic study. These data provide evidence for usefulness of IG in preventing the consequences of catecholamine excess in acute stage of MI.
...
PMID:Effectiveness of insulin-glucose in preventing adrenaline-induced myocardial and systemic disturbances in the dog. 699 26

It has been shown that a single intravenous injection of obsidan (0.1 mg/kg) to dogs during acute coronary occlusion results in a decrease in the activities of "a" phosphorylase, Mg-dependent ATPase, creatine phosphokinase, succinate dehydrogenase and cytochrome-c-oxidase, in a slight lowering of the ATP content accompanied by the increased content of AMP and unchanged concentration of creatine phosphate. Repeated injections of the drug in the same dose raise the activities of the enzymes up to the control level and produce activation of glycogenolysis and succinate dehydrogenase during the reparative period. The drug favours the preservation of "b" phosphorylase activity in the infarcted tissue and does not change the content of adenine nucleotides and creatine phosphate upon prolonged application.
...
PMID:[Effect of prolonged beta-adrenergic blockade on myocardial energy metabolism in coronary occlusion]. 712 83

After chronic occlusion, collateral-dependent coronary arteries exhibit alterations in both vasomotor reactivity and associated myoplasmic free Ca(2+) levels that are prevented by chronic exercise training. We tested the hypotheses that coronary occlusion diminishes Ca(2+) uptake by the sarcoplasmic reticulum (SR) and that exercise training would prevent impaired SR Ca(2+) uptake. Ameroid constrictors were surgically placed around the proximal left circumflex (LCx) artery of female swine 8 wk before initiating 16-wk sedentary (pen confined) or exercise-training (treadmill run) protocols. Twenty-four weeks after Ameroid placement, smooth muscles cells were enzymatically dissociated from both the LCx and nonoccluded left anterior descending (LAD) arteries of sedentary and exercise-trained pigs, and myoplasmic free Ca(2+) was studied using fura 2 microfluorometry. After the SR Ca(2+) store was partially depleted with caffeine (5 mM), KCl-induced membrane depolarization produced a significant decrease in the time to half-maximal (t(1/2)) myoplasmic free Ca(2+) accumulation in LCx versus LAD cells of sedentary pigs. Furthermore, inhibition of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA; 10 microM cyclopiazonic acid) significantly reduced t(1/2) in cells isolated from the LAD but not from the LCx. Exercise training did not prevent the differences in t(1/2) myoplasmic free Ca(2+) accumulation observed between LCx and LAD cells. Occlusion or exercise training did not alter SERCA protein levels. These results support our hypothesis of impaired SR Ca(2+) uptake in coronary smooth muscle cells isolated distal to chronic occlusion. Impaired SR Ca(2+) uptake was independent of SERCA protein levels and was not prevented by exercise training.
...
PMID:Sarcoplasmic reticulum Ca(2+) uptake is impaired in coronary smooth muscle distal to coronary occlusion. 1140 89

Epidemiological data document that regular exercise protects against the morbidity and mortality associated with ischemic heart disease. Therefore, we tested the hypothesis that daily exercise (DE) increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion and alters the expression of calcium regulatory proteins. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. To test this hypothesis, we recorded the VAT in conscious sedentary normotensive, sedentary hypertensive, and DE hypertensive rats, and we associated these thresholds with the protein expression of the L-type calcium channel, Na+/Ca2+ exchanger, phospholamban, and sarco(endo)plasmic reticulum Ca(2+)-ATPase. Results document a significantly reduced time to ventricular arrhythmias (sedentary hypertensive, 3.7 +/- 0.3 min vs. sedentary normotensive, 4.8 +/- 0.3 min), an increased Na+/Ca2+ exchanger protein expression (47%), and a decreased phospholamban protein expression (-34%) in conscious hypertensive rats. DE increased the VAT (5.9 +/- 0.2 min), decreased the protein expression of the Na+/Ca2+ exchanger, and normalized the protein expression of phospholamban in the hypertensive rats. Thus DE may be a primary prevention approach for reducing the incidence of arrhythmias by altering calcium regulatory proteins in hypertensive rats.
...
PMID:Daily exercise-induced cardioprotection is associated with changes in calcium regulatory proteins in hypertensive rats. 1547 72

Myocardial ischemia/reperfusion (MI/R) injury has a great influence on the prognosis of patients with acute coronary occlusion. The underlying mechanisms of MI/R injury are complex. While the incidence of MI/R injury is increasing every year, the existing therapies are not satisfactory. Recently, small ubiquitin-related modifier (SUMO), which is a post-translational modification and involved in many cell processes, was found to play remarkable roles in MI/R injury. Several proteins that can be SUMOylated were found to interfere with different mechanisms of MI/R injury. Sarcoplasmic reticulum Ca²⁺ ATPase pump SUMOylation alleviated calcium overload. Among the histone deacetylase (HDAC) members, SUMOylation of HDAC4 reduced reactive oxygen species generation, whereas Sirt1 played protective roles in the SUMOylated form. Dynamic-related protein 1 modified by different SUMO proteins exerted opposite effects on the function of mitochondria. SUMOylation of hypoxia-inducible factors was fundamental in oxygen homeostasis, while eukaryotic elongation factor 2 SUMOylation induced cardiomyocyte apoptosis. The impact of other SUMOylation substrates in MI/R injury remains unclear. Here we reviewed how these SUMOylated proteins alleviated or exacerbated myocardial impairments by effecting the MI/R injury mechanisms. This may suggest methods for relieving MI/R injury in clinical practice and provide a reference for further study of SUMOylation in MI/R injury.
...
PMID:Roles and mechanisms of SUMOylation on key proteins in myocardial ischemia/reperfusion injury. 3134 68


<< Previous 1 2

---