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)

The activity of the erythrocyte enzymes: glucose-6-phosphate dehydrogenase, pyruvate kinase, glutathion reductase and ATPase were measured in 8 patients with untreated myelomatosis. Glucose-6-phosphate dehydrogenase was significantly increased. Glucose-6-phosphate dehydrogenase values were negatively correlated with the glomerular filtration rate as measured by 51Cr-EDTA clearance. The results support the existence of a shortened red cell survival in peripheral blood related to the degree of renal insufficiency.
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PMID:Erythrocyte enzymes in myelomatosis. 13 47

Endogenous factors with biological and immunological activity similar to cardiac glycoside drugs (endogenous digitalis-like factors; EDLF) have been found in several tissues and body fluids of animals and humans. Detectable EDLF concentrations were found in blood and urine extracts of adults (normal healthy controls, hypertensive patients and salt-loaded healthy subjects), while higher levels were generally observed in plasma samples of pregnant women, newborns, and patients with renal insufficiency. The chemical characteristics of this endogenous factor are, at present, unknown, although it has been suggested that EDLF could be a substance with low molecular weight. Experimental studies and theoretical considerations suggest that EDLF, in addition to the ability to react with antibodies, might also bind to the specific cellular receptor of the cardiac glycosides and thus inhibit the membrane Na+/K(+)-ATPase (sodium pump). Therefore, it has been suggested that EDLF is an endogenous modulator of the membrane sodium-potassium pump, and that it could play a role in the regulation of fluids and electrolytes, in the myocardial muscular tone and also in the pathogenesis of hypertension.
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PMID:Endogenous digitalis-like factors: their possible pathophysiological implications with particular regard to the perinatal period. 196 38

Diabetics have an increased risk of developing renal insufficiency, as well as congestive heart failure independent of coronary atherosclerotic or hypertensive heart disease. Aluminum toxicity is being recognized with increased frequency in patients with reduced renal function and aluminum accumulates to a greater degree in tissues of patients with diabetes. Studies in patients with end stage renal disease have implicated aluminum overload as a potential cause of reduced cardiac function. Since both diabetes and aluminum decrease the activity of (Ca + Mg)-ATPase, a key enzyme involved in myocardial calcium transport, the interaction of experimental diabetes mellitus and aluminum toxicity on myocardial sarcoplasmic reticulum calcium transport was investigated in rats. Aluminum alone had no effect on (Ca + Mg)-ATPase activity, while activities in both the diabetic ([DM]) and diabetic plus aluminum loaded ([DM + Al]) groups were significantly lower than controls ([C]). Oxalate-dependent calcium uptake in the [DM] rats was slightly, but not significantly lower than controls, however, uptake was markedly reduced in rats which were both diabetic and aluminum loaded. The calcium regulatory protein calmodulin was measured by a functional assay in the soluble fraction of myocardial tissue prepared from each of the four groups. Compared to [C], calmodulin activity was significantly reduced in both the [DM] and [DM + Al] groups but not affected by aluminum alone. These data indicate that diabetes mellitus is associated with decreased myocardial calmodulin activity that may contribute to reduced sarcoplasmic reticulum (Ca + Mg)-ATPase and calcium transport activities and that aluminium toxicity potentiates the adverse effects of diabetes on decreasing sarcoplasmic reticulum calcium uptake.
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PMID:Effects of diabetes mellitus and aluminum toxicity on myocardial calcium transport. 214 51

Endogenous digitalis-like factors have been implicated in the adaptations that accompany renal insufficiency and in the pathogenesis of hypertension. We recently described several fractions of normal human plasma that inhibit NaK-ATPase and exhibit apparent digoxin-like immunoreactivity. To determine if hypertension and/or renal insufficiency affect plasma levels of these factors, we examined four patient groups: normotensive controls; hypertensive subjects with normal renal function; hypertensives with moderate renal insufficiency; and chronic dialysis patients. Plasma levels of digoxin-like immunoreactivity and NaK-ATPase inhibitory activity were significantly increased in hypertensive patients with mild renal failure (7.6 +/- 1.1 ouabain equivalents, mean +/- SEM, N = 21 vs 4.1 +/- 1.1 in normotensive controls, N = 20, P less than 0.05). NaK-ATPase inhibitory activity tended to be higher in patients with primary hypertension and normal renal function (5.5 +/- 0.7 ouabain equivalents, P less than 0.07); in dialysis patients, it was not different from controls. There was no correlation between NaK-ATPase inhibitory activity and blood pressure in any group. There was a significant rise in plasma NaK-ATPase inhibitory activity during dialysis (+ 1.8 +/- 0.7 ouabain equivalents, N = 22, P less than 0.03). As we have found that NaK-ATPase inhibitory activity in the plasma of normal humans can be separated into three distinct fractions, EI1, EI2, and EI3, we analyzed the plasma of 10 dialysis patients further. The increase in NaK-ATPase inhibitory activity could be attributed to fractions EI1 and EI3. These results suggest that plasma NaK-ATPase inhibitors increase with chronic renal insufficiency, but not hypertension alone. Although hemodialysis may acutely raise plasma levels, long-term dialysis returns them to the normal range.
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PMID:Endogenous digitalis-like factors in hypertension and chronic renal insufficiency. 302 36

The energy metabolism of kidney and renal function were studied in rats following an IV injection of living Escherichia coli. Energy charge (ATP + 0.5 ADP/ATP + ADP + AMP) decreased throughout the period studied. Total and ouabain-sensitive Na-K ATPase activity of renal cortex homogenate decreased markedly at 3 hr followed by gradual recovery. Polyulia was seen at 3 and 6 hr followed by oliguria at 12 hr after E. coli injection. PSP excretion test showed a marked decrease throughout the time course. In contrast, creatinine clearance decreased only at 12 hr. From these results, it was clarified that the renal insufficiency following bacteremia occurs in two different stages; the early stage with a high urinary output accompanied by decreased Na-K ATPase activity suggesting deterioration of proximal tubular functions and the late stage with oliguria in which glomerular filtration is severely depressed. In both stages, renal energy metabolism is markedly disturbed.
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PMID:Pathophysiology of acute renal failure following living Escherichia coli injection in rats: high-energy metabolism and renal functions. 303 71

Six patients with varying degrees of renal insufficiency developed severe hyperkalemia following hepatic necrosis. The hyperkalemia was seen prior to or concomitant with marked elevations in hepatic enzymes. The basis of the liver disease appeared to involve congestive heart failure and/or hypotension. Necrotic liver cells released intracellular potassium into the blood of patients who were unable to handle the additional potassium load because of renal insufficiency and metabolic acidosis. Furthermore, a shift of potassium into the intracellular space is impaired in uremics by defective Na-K ATPase activity, possibly induced by uremic toxins. The 3 diabetic patients in our series may additionally have had aldosterone deficiency leading to impaired cellular potassium uptake.
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PMID:Hyperkalemia provoked by acute hepatic necrosis. 377 39

The digitalis-like activities of plasma extracts from 108 patients and normal subjects were measured by their ability to compete with ouabain for binding to the digitalis sites of the Na+-pump. High levels were found in 18 of 54 untreated patients with moderate hypertension, 10 of 14 patients with end-stage renal failure and six patients with active acromegaly. These levels returned to control values after dialysis in the patients with renal insufficiency and high levels of the inhibitor, and after successful surgery and cobalt therapy in seven acromegalic patients. An increase in circulating Na+, K+-ATPase inhibitor was also found in rats after chronic sodium loading. These results indicate that levels of the circulating compound with digitalis-like properties do not result from high blood pressure but, rather, are related to blood volume and Na+ balance.
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PMID:Investigation of the endogenous Na+-pump inhibitor in essential hypertension and blood volume expansion. 610 Jul 47

25-Hydroxyvitamin D3 1 alpha- and 24-hydroxylase, NADPH-cytochrome c reductase, heme oxygenase, and ATPase activities were studied in viable kidney cells isolated from rats submitted to unilateral kidney damage (cortical electrocoagulation) and during the development of acute renal failure subsequent to excision of the contralateral undamaged kidney. Measurements of blood pH, plasma total and ionized calcium, phosphorus, creatinine, kidney histology, and phosphorus nuclear magnetic resonance spectroscopy determinations of phosphorus-containing compounds in kidney tissue were also performed. Seventy-two hours after unilateral kidney damage, no significant changes were observed in blood pH or in the plasma parameters studied. During this period, a significant increase in the activity of the 25-hydroxyvitamin D3 hydroxylases could be demonstrated in the cells of the contralateral undamaged kidney. A similar pattern of compensatory rise in the activity of the other enzymes studied was not detected. However, in the damaged kidney viable cells, the hydroxylase activities remained unchanged relative to those in sham-operated controls, despite a 5-fold increase in the inorganic phosphate content and a marked decrease in the organophosphorus and ATP content of this tissue. During the development of acute renal failure, a significant decrease in the activity of the hydroxylases occurred only when the rise in plasma creatinine concentration suggested severe renal insufficiency.
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PMID:Changes in 25-hydroxyvitamin D3 alpha- and 24-hydroxylase activities of kidney cells isolated from rats with either unilateral kidney damage or acute renal insufficiency. 622 3

We investigated whether urinary excretion of free dopamine is related with the humoral factors which affect Na+, K+ ATPase activity in the kidneys. Subjects were 51 adults admitted in a hospital without renal insufficiency: they were divided into normotensive (n = 36, 60 +/- 3 years old, 122 +/- 3/73 +/- 2 mmHg) and hypertensive groups (n = 15, 65 +/- 5 years old, 157 +/- 6/91 +/- 2 mmHg). Urinary excretion of free dopamine was significantly and positively correlated with urinary excretion of C-peptide immunoreactivity of insulin (CPR) (r = 0.451, p = 0.014) in normotensive subjects, but not in hypertensive subjects (r = 0.155, p = 0.668). Urinary excretion of endogenous digoxinlike substances (EDLS) was also significantly and positively correlated with urinary CPR (r = 0.500, p = 0.006) in normotensive subjects, but not in hypertensive subjects (r = 0.275, p = 0.363). In normotensive subjects, urinary excretion of free dopamine and EDLS may be regulated at least in part by insulin secreted endogenously. In hypertensive subjects, however, this regulatory mechanism of the diuretic factors, such as insulin, EDLS and dopamine, is thought to be deranged, which might result in decompensation of a diuretic and antidiuretic balance leading to blood pressure elevation.
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PMID:Urinary excretion of free dopamine and digoxinlike substances correlates with endogenous secretion of insulin in normotensive adults, but not in hypertensive subjects. 852 59

Gastro-oesophageal reflux disease (GORD) is a very common disorder of upper gastro-intestinal motility, differing widely in severity and prognosis. Medical therapy of GORD has involved antacids, alginates, prokinetic agents and antisecretory compounds, primarily H2 receptor antagonists and proton pump inhibitors. Knowledge of the pharmacokinetics of these compounds is important, to optimise the therapeutic benefit in each patient. GORD patients are often elderly and pharmacokinetics are move variable in this group. Furthermore, they often suffer from other diseases needing medical therapy and may need a combination of drugs to heal reflux oesophagitis and relieve reflux symptoms. The ideal therapy for GORD will have linear pharmacokinetics, a relatively long plasma half-life (t1/2), a duration of action allowing once daily administration, and a stable effect independent of interactions with food, antacids and other drugs. Over-the-counter antacids and alginates are widely used, buy may affect absorption of H2 receptor antagonists like cimetidine and ranitidine. Aluminium-containing antacids may, over time, cause toxicity in patients with renal insufficiency. In the treatment of GORD, cisapride presents important advantages over earlier prokinetic compounds, with a longer plasma t1/2, low penetration of the blood-brain barrier and fewer adverse effects. The group of H2 receptor antagonists is still the most frequently use therapy for GORD. Linear pharmacokinetics make dose adjustments easy and safe. In individual patients, suppression of gastric secretion is related to the area under the plasma concentration-time curve (AUC), but there is wide interindividual variation in the effect of the same oral dose. Only with frequent administration and high doses will acid suppression approximate that of proton pump inhibitors. Tolerance, with loss of effect over time, however, is most pronounced in this situation. H2 receptor antagonists seem well suited for on-demand treatment of reflux symptoms, due to the rapid onset of effect and a decrease likelihood of the development of tolerance. Effervescent formulations provide more rapid absorption and almost immediate clinical effect. Cimetidine, however, causes interference with the metabolism of several other drugs in common use. In elderly patients elimination is delayed and in patients with renal insufficiency, dose reductions of all H2 receptor antagonists are recommended. The most effective medical therapy for any severity of GORD, particularly in severe oesophagitis, are the proton pump inhibitors. The substituted benzimidazoles (omeprazole, lansoprazole and pantoprazole), are prodrugs which once trapped and activated in the acid milieu of the gastric glands potently suppress gastric secretion of acid and pepsin. Their long duration of action, more related to the slow turnover of parietal cell H(+)-K+ ATPase molecules, allows once daily administration in most patients. Interindividual variation in bioavailability sometimes calls for higher doses or twice daily administration. Acid suppression is closely related to the AUC. Omeprazole is prone to interaction with the metabolism of other drugs, some of which may e be clinically important. Lansoprazole seems to have an earlier onset of action than omeprazole, ascribed to higher bioavailability during the first days of treatment. Proton pump inhibitors have a slow onset of action, which makes them unsuited for on-demand therapy. Clinical practice in GORD calls for the use of not one but several substances, according to the severity and symptom pattern of the patient. Pharmacokinetic optimisation in the treatment of GORD is a question of selecting the most suitable substances and administration schemes within each group. Cisapride is superior to other prokinetics in terms of longer plasma t1/2 and less toxicity. Amongst H2 receptor antagonists, the more long-acting compounds, ranitidine and famotidine, will improve acidity control througho
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PMID:Pharmacokinetic optimisation in the treatment of gastro-oesophageal reflux disease. 911 86


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