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)

Studies in rats have shown that fecal potassium excretion and colonic mucosa Na-K-ATPase activity are elevated during dietary potassium loading and in chronic renal insufficiency. We studied Na-K-ATPase activity in human rectal mucosa in normal subjects as well as in patients with chronic renal insufficiency (creatinine clearance 2 to 72 mL/min). In normals, Na-K-ATPase activity was 4.34 +/- 0.83 mumol P/mg protein. After 2 weeks on a potassium intake of 300 mmol/d the mean activity did not differ significantly from the control value (2.49 +/- 1.30). In none of the patients with renal failure was Na-K-ATPase activity beyond the range found in the normal subjects, irrespective of serum potassium; the mean activity was 3.50 +/- 0.85. Like others, however, we found a two-fold increase in Na-K-ATPase activity in potassium loaded rats. Possible explanations for these differences are discussed.
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PMID:Sodium potassium ATPase activity in human rectal mucosa with and without renal insufficiency. 298 40

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

An increase in endogenous Na+,K+-ATPase inhibitor(s) with digitalis-like properties has been reported in chronic renal insufficiency, in Na+-dependent experimental hypertension and in some essential hypertensive patients. The present study specifies some properties and some biochemical characteristics of a semipurified compound from human urine having digitalis-like properties. The urine-derived inhibitor (endalin) inhibits Na+,K+-ATPase activity and [3H]-ouabain binding, and cross-reacts with anti-digoxin antibodies. The inhibitory effect on ATPases of endalin is higher on Na+,K+-ATPase than on Mg2+-ATPase and Ca2+-ATPase. The mechanism of endalin action on highly purified Na+,K+-ATPase was compared to that of ouabain and was similar in that it reversibly inhibited Na+,K+-ATPase activity; it inhibited Na+,K+-ATPase non-competitively with ATP; its inhibitory effect was facilitated by Na+; K+ decreased its inhibitory effect on Na+,K+-ATPase; it competitively inhibited ouabain binding to the enzyme; its binding was maximal in the presence of Mg2+ and Pi; it decreased the Na+ pump activity in human erythrocytes; it reduced serotonin uptake by human platelets; and it was diuretic and natriuretic in rat bioassay. The endalin differed from ouabain in only three aspects: its inhibitory effect was not really specific for Na+,K+-ATPase; its binding to the enzyme was undetectable in the presence of Mg2+ and ATP; it was not kaliuretic in rat bioassay. Endalin is a reversible and partial specific inhibitor of Na+,K+-ATPase, its Na+,K+-ATPase inhibition closely resembles that of ouabain and it could be considered as one of the natriuretic hormones.
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PMID:Further biochemical characterization of an Na+ pump inhibitor purified from human urine. 302 85

The frequent occurrence of sensorineural hearing loss in patients with chronic renal insufficiency prompted us to study the influence of chronic renal failure upon Na+,K+-ATPase in the inner ear of guinea pigs. Na+,K+-activated ATPase was defined as the ouabain-sensitive part of total ATPase, the activity of which was obtained in the presence of sodium, potassium and magnesium. A significant reduction of Na+,K+-activated ATPase was found in the inner ear of uremic animals. Such inhibition could be demonstrated as early as 12 hours after subtotal nephrectomy. An inverse correlation was found between serum creatinine levels and Na+,K+-activated ATPase. A similar inhibition of Na+,K+-activated ATPase in uremia is also found in other tissues (erythrocytes, renal tubules, intestinal mucosal cells, sarcolemma). Na+,K+-ATPase in the cochlea plays a key role in the maintenance of cochlear cationic gradients. It is suggested that inhibition of this enzyme system may contribute to the inner ear dysfunction in uremia.
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PMID:Inhibition of Na+,K+-stimulated ATPase in the cochlea of the guinea pig. A potential cause of disturbed inner ear function in terminal renal failure. 625 27

After chronic dietary potassium loading, epithelia in distal portions of the nephron and large intestine adapt to increase the rate of potassium secretion. This response to increased excretory loads of potassium maintains overall external balance and protects against the potentially lethal effects of hyperkalemia. The cellular adaptation in epithelia involved in preserving potassium homeostasis during potassium loading is characterized by an increase in the number of potassium pumps, reflected by an increase in Na-K-ATPase activity, in the basolateral cell membrane due, at least in part, to an amplification in the area of this membrane, and by an increase in transepithelial potential difference in most, but not all, adapted epithelia. These changes suggest that potassium adaptation is due to a step-up in the rate of cell uptake of potassium. In addition to chronic dietary loading, other conditions such as chronic renal insufficiency, elevated levels of mineralocorticoids, and administration of glucocorticoids are also characterized by accelerated rates of potassium secretion in the distal nephron and colonic mucosa and stimulation of Na-K-ATPase in basolateral portions of the cell membrane. These cellular changes in epithelia with increased capacity for potassium secretion are discussed in the context of our present understanding of mechanisms that control potassium excretion in urine and feces.
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PMID:Mechanism of potassium adaptation. 705 49