Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythrocytes from 15 uremic children aged from 7 months to 16 years were analyzed for adenosine triphosphatase (total ATPase and ouabain sensitive ATPase i.e. Na+, K+-ATPase), sodium and potassium ions and ATP concentration, in some cases before and after therapeutic measures had been undertaken. No correlation was found between the levels of Na+, K+-ATPase and serum creatinine and all uremic children had Na+, K+-ATPase levels within the range for normal children. The children with rapidly progressive uremia had higher activities of Na+, K+-ATPase at the corresponding serum creatinine concentration than those with slowly progressive uremia. Longitudinally the Na+, K+-ATPase activities fell and the erythrocyte Na+-K+ ratio increased in slowly progressive uremia. Introduction of a low-protein, high-energy diet giving accelerated growth did not change the Na+, K+-ATPase activities, the concentrations of erythrocyte sodium and potassium ions or ATP. Hemodialysis gave a slight increase of Na+, K+-ATPase and of the erythrocyte Na+-K+ ratio, whereas renal transplantation resulted in a remarkable increase of Na+, K+-ATPase activity and decrease of Na+-K+ ratio. A distinct feature of uremic children with hypertension was a low erythrocyte Na+-K+ ratio and a high Na+, K+-ATPase level.
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PMID:Characteristics of active sodium and potassium transport in erythrocytes in children with different stages of symptomatic uremia. 645 27

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

Tetrandrine, an alkaloid extracted from the Chinese medicinal herb Radix stephania tetrandrae, has traditionally been used to treat hypertension. In the present study, the effect of tetrandrine on vascular smooth muscle was investigated by using the rat tail artery as a model of a resistance vessel. Tetrandrine relaxes the tension in tail artery helical strips produced by depolarization with 60 mM KCl. Further studies show that tetrandrine inhibits the KCl-induced intracellular Ca++ increase and L-type voltage-dependent Ca++ channel currents, suggesting that tetrandrine relaxes the vessel via inhibition of Ca++ influx through Ca++ channels. Tetrandrine also inhibits norepinephrine (NE)-induced vasocontraction in the presence of extracellular Ca++. It does not, however, inhibit NE-induced vasocontraction in the absence of extracellular Ca++. Tetrandrine also inhibits the NE-induced intracellular Ca++ increase in the presence of extracellular Ca++ and has no effect on the NE-induced intracellular Ca++ increase in the absence of extracellular Ca++. This suggests that tetrandrine also blocks NE-induced Ca++ influx but not NE-induced Ca++ release from the intracellular Ca++ stores. Furthermore, tetrandrine inhibits thapsigargin-induced intracellular Ca++ concentration increase, suggesting that, in addition to blocking Ca++ influx, tetrandrine also may interfere with the interaction between thapsigargin and Ca++ adenosine triphosphatase.
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PMID:Tetrandrine, a Ca++ antagonist: effects and mechanisms of action in vascular smooth muscle cells. 771 83

Although the pathogenesis of the diabetes mellitus syndrome remains poorly understood, both insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus predispose the individual to a similar spectrum of complications, including hypertension, macrovascular and microvascular disease, cataracts cardiomyopathy, neuropathy, and premature aging, suggesting that these complications develop along a pathway common to both diabetic conditions. Yet not all diabetic persons are affected by all of these complications or to the same degree. What causes this marked variability in the clinical manifestations of the diabetes syndrome remains an enigma. Accumulating data from animal models of diabetes and from studying patients with diabetes reveal that intracellular calcium levels are increased in most tissues. The activities of the membrane, adenosine triphosphatase (ATPase) associated cation pumps, which determine intracellular calcium level (i.e., calcium-ATPase and [sodium + potassium]-ATPase), are also altered. The nature of the alteration is often tissue specific and may depend on the level of blood glucose or insulin, or both. In this review we discuss the potential contribution of these changes in intracellular calcium regulation, whether acquired or genetically determined, to the pathogenesis of the diabetes syndrome, to the abnormalities in insulin secretion and action (mainly in non-insulin-dependent diabetes), and to the complications of both diabetes syndromes. Altered intracellular calcium metabolism may represent a common, underlying abnormality linking the metabolic, cardiovascular, ocular, and neural manifestations of the diabetic disease process.
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PMID:Diabetes mellitus: a disease of abnormal cellular calcium metabolism? 762 30

Circulating inhibitors of the transport enzyme, sodium-potassium-activated adenosine triphosphatase (Na(+)-K(+)-ATPase), have been shown to be of possible pathogenetic importance in the mechanism of essential hypertension. Although previous studies have demonstrated the presence of both high molecular weight (HMW) and low molecular weight (LMW) natriuretic plasma Na(+)-K(+)-ATPase inhibitors, no previous attempts have been made to ascertain whether HMW or LMW forms predominate in hypertension. In this study, plasma samples obtained from 26 patients with essential hypertension, 12 normotensive controls, and six normotensives with a family history of hypertension, were separated into HMW and LMW moieties by passage through a 1 kDa Amicon membrane. The LMW moiety was separated on C18 Sep-Pak cartridges, applying a 10% step-wise acetonitrile trifluoroacetic acid gradient. The HMW moiety was further separated on Sephadex G-75. Sodium dodecyl sulfate polyacrylamide gel electrophoresis revealed that the fraction with inhibitory activity contained a distinct 12 kDa protein band, with staining intensity depending on the presence or absence of hypertension. Na(+)-K(+)-ATPase inhibitory activity was found in several LMW fractions, but differences between hypertensives and normotensives were observed in only one fraction (0.29 +/- 0.12 SD v 0.11 +/- .12 mumol/L ouabain equivalents, P < .01). Na(+)-K(+)-ATPase inhibitory activity in the HMW fraction was 38 x the inhibitory activity in the LMW fraction and was significantly increased in hypertensives as compared to normotensive controls (10.9 +/- 8.9 v 1.3 +/- 0.8 mumol/L ouabain equivalents, P < .01). Inhibitory activity in both HMW and LMW fractions correlated positively with mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predominance of high molecular weight plasma Na(+)-K(+)-ATPase inhibitor in essential hypertension. 821 31

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

The effect of long-term treatment with propafenone, metoprolol and amiodarone was studied on the activity of Na,K-adenosine triphosphatase in lymphocytes and the plasma level of cAMP in patients with ventricular arrhythmias. The investigations were carried out in 86 patients with cardiac dysrhythmias caused by coronary artery disease, hypertension, post-inflammatory and alcohol cardiomyopathy and preexcitation syndrome. Propafenone was used in treatment in 31 patients, metoprolol in 30, amiodarone in 25. The activity of of Na,K-adenosine triphosphatase in lymphocytes was estimated by the method of Heagerty et al. The plasma level of cAMP was measured radioimmunologically. Disappearance of ventricular arrhythmias after treatment was accompanied by increase in activity of of Na,K-adenosine triphosphatase and decrease in plasma level of cAMP regardless of which drug was used. Ineffective treatment did not affect both parameters.
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PMID:[The effect of treatment with propafenone, metoprolol and amiodarone on lymphocyte sodium efflux and level of cAMP in serum]. 852 94

The Na+, K(+)-activated adenosine triphosphatase (ATPase) is present in the membrane of eukaryotic cells and represent a major pathway for Na+ and K+ transport across the plasma membrane. Cardiac glycosides, such as digoxin or ouabain, inhibit this enzyme activity by binding to a specific receptor on the membrane. Studies conducted in this and other laboratories have proven the existence of digitalis-like compounds in animal and human tissues which may serve as regulators, in vivo, of the Na+, K(+)-pump activity. The levels of digitalis-like compounds in the plasma are increased in hypertension and other illnesses. A possible link at the cellular and molecular level between these compounds and etiology of arrhythmias, an important cause of morbidity and mortality in patients with various diseases of the heart, can be postulated: Na+, K(+)-ATPase activity contributes directly and indirectly to the electrical membrane potential of cardiac cells. The inhibition of this pump by the endogenous digitalis-like compounds, in discrete areas of the heart, can induce changes of the membrane potential of these cells. These changes may cause an increase in excitability of the particular cells and contribute to the generation of arrhythmias.
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PMID:Na+, K(+)-ATPase and heart excitability. 854 Apr

Inhibitors of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) have been implicated in the pathogenesis of hypertension. In the study presented here, an attempt was made to determine whether differences in the plasma levels and the removal rates of high-molecular weight (HMW) and low-molecular weight (LMW) forms of Na-K-ATPase inhibitors might relate to blood-pressure control in hemodialysis (N = six ultrafiltered and N = six non-ultrafiltered) and CAPD (N = six long-term and N = five short-term) patients. The latter group was studied before the initiation of continuous ambulatory peritoneal dialysis (CAPD) and 2 wk after starting the treatment. The mean blood pressure was significantly reduced after dialysis in the nonultrafiltered hemodialysis group and in both CAPD groups. Plasma levels of both HMW and LMW inhibitors were found to be elevated before dialysis in all patients and were modified only slightly after dialysis. Irrespective of whether ultrafiltration was utilized in hemodialysis patients and despite significant losses of both HMW and LMW inhibitors into CAPD effluent. Because CAPD effluent was found to contain vasopressors that were not exclusively Na-K-ATPase inhibitors, losses of these other vasopressors may contribute to improved blood-pressure control in CAPD in contrast to hemodialysis.
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PMID:Relationship of Na-K-ATPase inhibitors to blood-pressure regulation in continuous ambulatory peritoneal dialysis and hemodialysis. 870 12

To determine a possible role of sodium-potassium adenosine triphosphatase (Na+, K+-ATPase) in the regulation of membrane functions in hypertension, we investigated the effects of ouabain on the membrane fluidity of erythrocytes in spontaneously hypertensive rats (SHR) by means of an electron paramagnetic resonance (EPR) and spin labeling method. Erythrocytes obtained from SHR were examined compared with age matched Wistar-Kyoto (WKY) rats, and the EPR spectra for 5-nitroxide stearate incorporated into the erythrocyte membranes were studied. The value of order parameter (S) of the EPR spectra was significantly higher in the erythrocytes of SHR than in the erythrocytes of WKY rats (S value: SHR, 0.721+/-0.009, n = 10; WKY, 0.652+/-0.008, n = 10; P < .05). The finding shows that the membrane fluidity of erythrocytes was lower in SHR than in WKY rats. Ouabain loading to erythrocytes significantly decreased the membrane fluidity (S value was increased) in both SHR and WKY rats. The ouabain induced change was significantly greater in SHR than in WKY rats. These results demonstrate that the membrane fluidity of erythrocytes might be highly dependent on the Na+, K+-ATPase activity in SHR, which would suggest an abnormality in Na+ related cellular functions in hypertension.
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PMID:The role of sodium-potassium adenosine triphosphatase in the regulation of membrane fluidity of erythrocytes in spontaneously hypertensive rats: an electron paramagnetic resonance investigation. 944 78


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