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

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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)

Activity of Na+, K+-ATPase and the molar ratio "cholesterol/phospholipids" were estimated in erythrocyte membranes of patients with ischemic heart disease, in which an impairment of coronary arteries was documented by means of angiography. Distinct inhibition of the enzymatic activity as well as an increase in the ratio "cholesterol/phospholipids" was observed in erythrocyte membranes of all the patients; the alteration of these parameters was maximal in the patients with IIa and IIb forms of hyperlipoproteinemia. Reverse correlation (r = -0.604) was found between the enzymatic activity in erythrocyte membranes and the "atherogeneity coefficient" in blood plasma lipoproteins. The data obtained suggest that blood plasma lipoproteins are responsible for regulation of cholesterol content in cell membranes and, according to the membrane hypothesis of atherogenesis, this phenomenon is important in development of atherosclerosis.
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PMID:[Na+, K+-ATPase activity and cholesterol content in erythrocyte membranes of patients with coronary atherosclerosis in various forms of dyslipoproteinemia]. 631 64

Parallel stereo- and cytospectrophotometric examinations of human myocardial capillaries, 20-60 min after biological death were carried out. The activity of alkaline phosphatase, adenosine triphosphatase, lactate dehydrogenase and NAD-diaphorase in the capillary wall in relation to the sex and age in cardiovascular pathology, renal diseases and leukemias were studied. The permeability and level of energy supply of transendothelial transport were found to depend on the kind of the main pathological process and type of death. According to the parameters under study, the functional state of the capillary network of the myocardium in atherosclerosis with or without its combination with hypertension and also in secondary renal hypertension is described.
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PMID:[Stereological characteristics and enzymatic activity of myocardial capillaries in different variants of pathology and death (data from immediate autopsies)]. 686 Jan 68

The object of this study was to examine changes in plasma membranes of arterial smooth muscle (ASM) during atherogenesis obtained from cholesterol-fed (2%) rabbits. A microsomal fraction highly enriched with plasma membrane markers was prepared by subcellular organelle fractionation from ASM freshly isolated from the thoracic aorta. The membranes were analyzed for unesterified (free) cholesterol (FC) content, membrane bilayer structural parameters (X-ray diffraction), phospholipid (PL) composition, and Na+/K(+)-ATPase activity and kinetics. Following 8 weeks on diet, membrane FC content increased 67.1%. Small angle X-ray diffraction demonstrated an increase in membrane hydrocarbon core electron density and an increase in overall lipid bilayer width (56-62 A). This increase in bilayer width was highly correlated with the membrane FC content (r = 0.992). Both membrane FC content And bilayer width independently correlated with time on cholesterol diet. The phospholipid profile of the membrane revealed a 16.4% increase in phosphatidylcholine (PC), 19.3% decrease in phosphatidylethanolamine (PE) and 62.8% increase in sphingomyelin (SM) content with no change in total PL content. Na+/K(+)-ATPase activity was decreased 52.2% (P < 0.005), and [3H]ouabain binding kinetics demonstrated a 27.6% decrease in maximum binding sites (Bmax) (P < 0.01) while the dissociation constant (Kd) remained unaltered. Membranes obtained from control ASM cells enriched with FC in culture demonstrated changes similar to those in atherosclerotic ASM membranes including an increase in membrane FC content, an increase in bilayer width, and a decrease in Na+/K(+)-ATPase activity with decreased ouabain Bmax. These data demonstrate marked compositional, structural and functional changes in ASM cell membrane characteristics in dietary atherosclerosis. These changes were highly correlated with cholesterol accumulation in the plasma membrane bilayer and were observed before the appearance of visible lesions. We suggest that these membrane defects may be linked with early atherogenesis.
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PMID:Atherosclerosis alters the composition, structure and function of arterial smooth muscle cell plasma membranes. 754 33

The activities of protein kinase C, total, Mg2 and Na+, K(+)-dependent ATPases in red cell membranes were compared in 46 patients with insulin independent, 30 ones with insulin dependent diabetes mellitus with various degrees of vascular disorders, and in 17 patients with atherosclerosis with the predominant involvement of the main vessels of the lower limbs. Diabetes mellitus and the progress of vascular disorders were associated with a more marked depression of protein kinase C, total and Na+, K(+)-dependent ATPase activities, this being particularly characteristic of the patients with insulin-independent diabetes and macrovascular disorders. Inhibited activities of protein kinase C and ATPases in red cell membranes in the course of diabetic vascular disorders progress evidence their contribution to the pathogenesis of diabetic angiopathy.
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PMID:[Activity of membrane-bound protein kinase C and ATPase in erythrocytes in diabetic angiopathy]. 805 53

Abnormal growth of vascular smooth muscle (VSM) is seen in various pathologic conditions such as hypertension and atherosclerosis. Many classic vasoconstrictors have now been shown to be mitogenic, either by themselves or in conjunction with other cofactors, such as insulin. The mitogenic effects of vasoconstrictors may be due, in part, to activation of similar second messenger pathways, including stimulation of the Na+/H+ antiporter. It has been suggested, therefore, that an enhanced proliferation rate may be, in part, the consequence of elevated Na+/H+ exchange. This hypothesis is supported by several observations of the close association between Na+/H+ exchange activity and DNA synthesis in some cell types including fibroblasts and VSM. Stimulation of Na+/H+ exchange may play a permissive role in optimal growth by preventing H+ accumulation (a fall in intracellular pH [pHi]) due to the increased metabolic activity during cell stimulation. Enhancement of Na+/H+ exchange activity increases Na+ influx into the cell, and secondarily increases K+ entry through activation of Na+/K+ ATPase activity. Although the Na+/H+ antiporter may influence cell proliferation through various ionic mechanisms, it is not clear that enhanced proliferation is the consequence of overactivity of this antiporter. In VSM, there are also differences in the pattern of activation of the Na+/H+ antiporter by hyperplastic and hypertrophic agents. Although pHi is increased in response to both acute and chronic stimulation by hyperplastic factors, such as platelet-derived growth factor, a hypertrophic agonist such as angiotensin II increases pHi acutely but lowers it chronically. Likewise, hyperplastic factors increase the Na+/H+ antiporter (NHE-1) mRNA levels, whereas angiotensin II does not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na+/H+ exchange and vascular smooth muscle proliferation. 814 Nov 73

Endothelial cell integrity has been suggested to play a role in the development of atherosclerosis. The effects of fatty acids on endothelial barrier function were tested by measuring albumin transport across endothelial monolayers cultured on polycarbonate filters. Compared with control cultures, a 24-h exposure to 90 mumol/L lauric (12:0) and linoleic acid (18:2) but not to butyric (4:0), hexanoic (6:0), octanoic (8:0), decanoic (10:0), myristic (14:0), palmitic (16:0) or stearic acid (18:0) caused an increase in albumin transfer across endothelial monolayers. Selective enrichment of a "physiological" serum fatty acid mixture (FA-Mix; 90 mumol/L) with 90 mumol/L of 12:0 or 18:2 significantly increased albumin transfer, whereas enrichment with 90 mumol/L of 4:0, 16:0 or 18:0 significantly decreased albumin transfer relative to 180 mumol/L FA-Mix. Only 12:0- or 18:2-treated cultures showed increased Ca(++)-ATPase activity and the presence of lipid droplets. Fatty acids (60 mumol/L) extracted from butter fat and beef tallow had no effect on albumin transfer, whereas fatty acids extracted from chicken fat and corn oil consistently disrupted endothelial barrier function. This fat-induced disruption of endothelial barrier function seems to be related to the amount of 18:2 present in each fat source. These data indicate that unsaturated fats cause cellular perturbations that result in a decrease in endothelial barrier function in this model system, and that high dietary levels of unsaturated fats may be detrimental to cell integrity.
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PMID:Selective disruption of endothelial barrier function in culture by pure fatty acids and fatty acids derived from animal and plant fats. 832 May 62

For more than a decade, the inhibition of the renin-angiotensin system in heart failure has been regarded as pure vasodilator therapy. Consequently, the role of the renin-angiotension system has been seen as contributing to hemodynamic overload by vasoconstriction and volume retention. Meanwhile, clinical experience was indicated that important additional aspects of ACE-inhibition in heart failure are attenuation of the enhanced neuroendocrine activity and reversal or prevention of inappropriate trophic reactions of the overloaded myocardium. In overloaded hearts there is enhanced intracardiac formation of angiotensin due to enhanced expression of angiotensinogen and ACE, and due to accumulation of circulating, nephrogenic active renin. In human hearts, a mast-cell-derived chymase, which is not blocked by ACE-inhibition, contributes to intracardiac angiotensin formation. The enhanced intracardiac angiotensin-II formation in overloaded hearts is involved in coronary constriction, impairment of diastolic relaxation, myocyte enlargement and interstitial fibrosis, which aggravate the diastolic impairment. The major problem in overloaded, hypertrophied cardiocytes is the dedifferentiation with instabilization of Ca(++)-homeostasis due to an altered program of gene expression. Dedifferentiated cardiocytes have a reduced expression of sarcoplasmic reticulum Ca(++)-ATPase and an enhanced expression of the sarcolemmal Na+/Ca(++)-exchanger, resulting in an attenuation of active diastole (Ca(++)-reaccumulation into the sarcoplasmic reticulum), a depressed force-frequency relation, and an enhanced susceptibility for fatal arrhythmias. Furthermore, an enhanced local renin-angiotensin system in distensible coronary and systemic arteries seems to contribute to a reduced releasability of endothelium-derived relaxing factor, probably by reducing bradykinin availability. This modulation of endothelial function appears to contribute to the localization and progression of atheroma development in presence of risks factors for atherosclerosis.
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PMID:Pathophysiology of heart failure and the renin-angiotensin-system. 835 33

The cells within the vascular wall act as a unit regulating the contraction of smooth muscle cells. In arteries the endothelium and autonomic nerves provide the major factors that regulate intracellular calcium in smooth muscle cells, which determines contractile tone. The endothelium provides a major inhibitory influence, which itself is modulated by shear forces within the vascular lumen regulating endothelial cell calcium and the release of endothelium-derived relaxing factors. Of the major mechanisms controlling smooth muscle calcium, it has been suggested that voltage-dependent calcium channels are among the most important in mediating the inhibitory influence of the endothelium. Smooth muscle potassium channels and sodium-potassium adenosine triphosphatase (Na+,K(+)-ATPase) are important regulators of membrane potential, and each is affected by the endothelium. Because the activity of each hyperpolarizes the membrane potential, they counter the influence on voltage-dependent calcium channels and inhibit contraction. Both of these counterregulatory mechanisms have recently been shown to be impaired in diseased arteries. This may help to explain the diminished effectiveness of the endothelium on the smooth muscle. Thus, vascular disease may cause diminished release, increased destruction, or limited effectiveness of endothelium-derived relaxing factors. The failure of the inhibitory influence of the endothelium may be the principal mechanism by which vascular risk factors and disease increase vasoconstrictor tone, possibly contributing to hypertension and the progression of atherosclerosis.
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PMID:Pathways controlling healthy and diseased arterial smooth muscle. 837

Both atherosclerotic lesions and hypoxia alter the contractile properties of the arterial wall and, in particular, may interfere with the relaxation mechanisms dependent or not on the endothelium. The present study was designed to test the effect of severe hypoxia on the contractile behavior of the atherosclerotic rabbit aorta. Segments of aortas obtained from control, cholesterol-fed, or Watanabe hereditary hyperlipidemic rabbits were mounted in organ chambers for isometric tension recording. A change of the bath PO2 from "normoxic" conditions (95% O2-5% CO2) to "hypoxic" conditions (95% N2-5% CO2) caused relaxation in the precontracted control aortas (by approximately 85%) but a transient contraction (approximately 20% of the maximal contraction obtained with 30 mM KCl) followed by a relaxation in the precontracted atherosclerotic aortas. Both types of responses were observed in aortas contracted with aggregating platelets, 5-hydroxytryptamine (5-HT), norepinephrine, endothelin, and prostaglandin F2 alpha. The hypoxic contractions in atherosclerosis were not dependent on the presence of an intact endothelium. They could not be antagonized by blockers of alpha-adrenoceptors, 5-HT2 receptors, histamine receptors, thromboxane receptors, and muscarinic cholinoreceptors. Inhibitors of cyclooxygenase, lipoxygenase, Na+, K(+)-ATPase, and free radical scavengers or an activator of endothelium-derived relaxing factor did not significantly affect the hypoxic contraction; the absence of effect of some inhibitors of protein synthesis seems to rule out the involvement of endothelin, angiotensin II, and bradykinin. The hypoxic contraction was not influenced by omission of Ca2+ from the medium or by inhibition of Ca2+ influx but was prevented by blockade of intracellular Ca2+. The inhibitor of nitric oxide synthase (nitro-L-arginine, 100 microM) and the guanylyl cyclase inhibitor (methylene blue, 10 microM) both enhanced the initial contractile responses to 5-HT to a similar extent as hypoxia and completely prevented the hypoxic contraction in the atherosclerotic tissues. The cyclic nucleotide analogues 8-bromo-cGMP and dibutyryl cAMP also inhibited the hypoxic contraction in the atherosclerotic aorta. The cGMP levels were markedly decreased and the cAMP levels were moderately decreased in the aortas of the cholesterol-fed rabbits as compared with the control aortas. Hypoxia further decreased cGMP but not the cAMP levels in atherosclerotic aortas with and without endothelium. Our data thus demonstrate the occurrence of an unusual vasoconstrictor response in atherosclerotic arteries; this constrictor response depends on the availability of intracellular Ca2+ and seems to be due to the further inhibition of an already impaired cGMP production.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxia causes an abnormal contractile response in the atherosclerotic rabbit aorta. Implication of reduced nitric oxide and cGMP production. 838 23

Endothelial cells play a pivotal role in the development of atherosclerosis. An 'activated' phenotype of these cells is manifested by signal transduction-dependent expression of genes encoding cytokines, pro- and anticoagulant factors, and cell adhesion molecules. In the current study we examined the effect of ouabain, an inhibitor of Na+/K(+)-ATPase, on the process of endothelial cell activation. We demonstrated that ouabain was able to stimulate VCAM-1 expression and potentiate the effect of IFN-gamma on this process. Moreover, ouabain provided a complementary signal for either TNF or IFN-gamma in inducing iNOS expression. Our data also show, for the first time, that inhibition of Na+/K(+)-ATPase led to activation of the transcription factor, NF-kappa B, which may provide an explanation for the effects of ouabain on endothelial cells.
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PMID:Stimulatory effect of ouabain on VCAM-1 and iNOS expression in murine endothelial cells: involvement of NF-kappa B. 854 10


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