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)

Penicillin pretreatment enhanced the rate of PAH uptake into separated proximal tubules (collagenase digestion) from 2-week New Zealand white rabbits. A double reciprocal plot of these data suggests that penicillin increases the maximal velocity of PAH uptake. Na, K-ATPase was less in adult tissue but was unaffected by penicillin. No ultrastructural changes could be attributed to the treatment. Thus substrate stimulation of PAH transport does not involve Na, K-ATPase and probably involves soluble, rather than structural proteins.
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PMID:Biochemical and ultrastructural correlates of substrate stimulation of renal organic anion transport. 13 21

In 1974, we found that sera from SHR suppressed renal PAH transport (PSEBM 145:97, 1974). Since a "natriuretic factor" depresses PAH as well as Na transport, we proposed that "natriuretic factor" was elevated in SHR. Our current investigation amplifies the previous study. On a given day, one spontaneously hypertensive rat (SHR) and one rat from a normotensive strain [Wistar Kyoto (WKY) or Sprague-Dawley (SD]) were examined together. SHR sera compared to WKY/SD sera significantly depress PAH (organic anion) and TEA (organic cation) uptake by rat renal slices. The ability of SHR sera to depress uptake correlated significantly with the BP: the sera with the greatest depressive influence on renal PAH and TEA uptake came from the SHR with the highest BP (PAH r = 0.89, p less than 0.0001; TEA = r = 0.76, p less than 0.01). Subsequent separation of serum on Sephadex 25 localized the factor to the same fraction as "natriuretic hormone". A similar correlation was found between the ability of the fraction to depress the 2 transports and the height of the BP. The serum factor did not inhibit ATPase activity. In contrast to the serum effects, renal slices removed from SHR showed increased rather than decreased PAH and TEA transport which significantly correlated with the BP. The slices with the highest uptakes came from the SHR with the highest BP. The high uptake of organic ions by the SHR renal slices could be an adaptive response to the serum factor or vice versa. We postulate that a serum factor which depresses PAH and TEA transport and is not "ouabain-like" may play a role in the BP elevation of SHR.
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PMID:Correlation of renal organic anion and cation transport with blood pressure in SHR. 165 69

Changes in renal function, Na+-K+-ATPase activity and PAH transport system in kidney cortex were studied in rats treated with cadmium. Subcutaneous injections of CdCl2 (2 mg Cd/kg.day) for 16 days induced a marked polyuria and a hyposthenuria. These changes were accompanied by increase in urinary protein, glucose, urea, calcium, phosphate, chloride and potassium excretions. The change in urine flow was proportional to the change in total osmotic solute excretion. Creatinine excretion and TcH2O remained unchanged. Na+ excretion was not increased, but the Na+-K+-ATPase of renal cortex was significantly inhibited. PAH uptake by renal cortical slices was markedly attenuated in Cd-treated rats. The Vmax for active PAH influx was drastically reduced, but the Km was not changed. The passive influx and efflux of PAH across the basolateral membrane and the renal tissue oxygen consumption were not apparently altered in Cd-treated animals. These results indicate that 1) the nature of Cd-induced polyuria and hyposthenuria is an osmotic diuresis induced by proximal tubular rejection of various substances, and 2) the mechanism of impaired renal PAH excretion in Cd-treated animals is a loss of organic anion carriers in proximal tubular basolateral membranes.
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PMID:Changes in renal function in cadmium-intoxicated rats. 285 38

Recovery of various parameters of kidney function after varying periods of complete unilateral ureteral obstruction was studied in dogs under hydropenic conditions. Changes of PAH and inulin clearance appeared to be parallel. After one week of obstruction, renal clearances of PAH and inulin were decreased to seven per cent of values measured before the obstruction period, after two weeks to four per cent and after three or four weeks to two per cent. Within 10 to 28 days after release of obstruction by cutaneous ureterostomy, PAH and inulin clearance increased to 66 per cent after one week, to 50 per cent after two weeks, to 10 per cent after three weeks with no change after four weeks of obstruction. Na+ content in the hydronephrotic kidney differed from contralateral kidneys only in the inner medulla. The affinity for ouabain (dissociation constant, KD, normal = 3.85 X 10(-9) M; hydronephrotic = 3.05 X 10(-9) M; contralateral = 7.05 X 10(-9) M) was significantly higher only in the outer medulla of contralateral kidneys. Turnover number (normal = 3.6; hydronephrotic = 5.1; contralateral = 3.4 X 10(3) min.-1) in hydronephrotic or contralateral outer medulla was not significantly different from normal. Changes in kinetic constants (association rate constant, k+1, normal = 4.49 X 10(4) M-1 sec.-1; hydronephrotic = 4.13 X 10(4) M-1 sec.-1; contralateral = 5.97 X 10(4) M-1 sec.-1; dissociation rate constant, k-1, normal = 1.03 X 10(-4) sec.-1; hydronephrotic = 1.29 X 10(-4)sec.-1; contralateral = 1.39 X 10(-4) sec.-1) were considered to be too small to be relevant. Similar changes of KD, k+1 and k-1 were observed in the renal cortex. The osmotic concentrating capacity correlated well with (Na+ + K+)-ATPase activity (r = 0.85) and number of 3H-ouabain binding sites (r = 0.89) in renal outer medulla. The results indicate that recovery of osmotic concentrating capacity depends on the length of obstruction, and that a reduction of (Na+ + K+)-ATPase molecules in the thick ascending limb of the loop of Henle is a primary factor in the decrease in the concentrating capacity of chronic unilateral hydronephrotic kidneys.
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PMID:Renal function and (NA+ + K+)-ATPase in chronic unilateral hydronephrosis in dogs. 300 70

Fatal immune complex glomerulonephritis can be induced in rats by chronic intravenous administration of bovine serum albumin. There are three distinct stages, mild, moderate, and severe, in the development of renal immunopathology and pathophysiology in this model of chronic serum sickness. The work described here was undertaken to evaluate aspects of proximal tubule function in those different stages. Tissue water distribution, oxidative metabolism, and transport of representative organic anions and cations were measured in renal cortical slices. In mild chronic serum sickness all functions were normal except the transport of p-aminohippurate (PAH, organic anion), which was significantly decreased. This decrease appeared to be attributable to immunization with Freund's adjuvant. In the moderate stage of chronic serum sickness, proximal tubule functions and morphology appeared essentially normal. Only Na-K-ATPase activity was somewhat lower than in controls. However, proximal tubule dysfunction was a feature of severe chronic serum sickness. A significant inhibition of anion and cation transport was observed. Reduction in transport functions occurred together with impaired oxidative metabolism and severe reduction in Na-K-ATPase activity. Abnormalities of mitochondrial structure, a decrease in number of mitochondria, and a significant increase in intracellular H2O content provided additional evidence of degenerative changes in proximal tubule cells during the severe stage of chronic serum sickness. It was concluded that decreased transport of organic ions by the basolateral membrane in proximal tubules of rats with severe chronic serum sickness resulted from a breakdown in the metabolic machinery of the tubule epithelium rather than a specific injury to organic ion transport systems.
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PMID:Proximal tubule function in chronic serum sickness glomerulonephritis of rats. 315 65

In this chapter are outlined the many factors involved in the regulation of sodium and volume homeostasis in normal human pregnancy and their interrelationships. New developments concerning the role of sodium/potassium ATPase, atrial natriuretic peptide, arginine vasopressin and angiotensin II as regulatory forces are outlined, together with a review of earlier work. Abnormalities found in women with, or destined for, PAH are described and their significance is discussed.
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PMID:Volume homeostasis in normal and hypertensive human pregnancy. 333 Apr 88

Renal tubular secretion of digoxin appears to be one of the main ports of elimination of the glycoside from the body. Because of its narrow therapeutic window and severe toxicity, the mechanisms of tubular handling of digoxin are important. Moreover, several drugs which are commonly administered with digoxin, including quinidine, spironolactone, verapamil and amiodarone have been shown to decrease renal clearance of digoxin without affecting GFR. We studied the handling of digoxin using in vitro and in vivo approaches. The handling of the glycoside by the brush border suggests passive reabsorption which is not enhanced by commonly coadministered drugs. Digoxin binding to the antiluminal (basal) membrane suggests that the secretion of the glycoside may not involve the pharmacologic receptor, the Na+, K+, ATPase. Using the multiple indicator dilution technique, we could directly show the two steps of secretion of digoxin: Its sequestration from the postglomerular circulation, and its appearance in the urine after transtubular transport. Digoxin transport is not inhibited by a cationic or anionic molecule (PAH and tolazoline). It is possible that digoxin is secreted by a yet unidentified transport mechanism.
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PMID:Cellular mechanisms of digoxin transport and toxic interactions in the kidney. 353 41

Basolateral membrane vesicles were isolated from the rat kidney cortex by a modified method of cation precipitation. Different steps of preparation were analysed using the marker enzymes: Na+,K+-ATPase (for basolateral membrane), alkaline phosphatase (for apical membrane), glucose-6-phosphatase (for membranes of endoplasmic reticulum) and succinate dehydrogenase (for mitochondria). The basolateral membrane was purified by a 8-9-fold treatment with Na+,K+-ATPase, while other membrane contaminations were as low as 2% (as compared to homogenate). The transport of 3H-p-aminohippurate (3H-PAH) by basolateral membrane vesicles was measured under different experimental conditions. The 3H-PAH uptake was found to be Na-gradient dependent. The initial rate of 3H-PAH uptake in the presence of NaCl gradient (500 pM/mg X min) was higher than without the gradient (88 pM/mg X min). It is concluded that the PAH transfer across the basolateral membrane may be energized by the Na+ chemical gradient.
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PMID:[Effect of a NaCl gradient on the transport of para-aminohippuric acid into the vesicles of the basolateral membrane of the kidney cortex]. 359 Mar 16

The bidirectional tubular transport of pyrazinoate (PZA) was studied in the isolated perfused proximal S2 segment of rabbit kidney. PZA reabsorption was a mechanism of large capacity, temperature-dependent and requiring a normal Na+/K+-ATPase activity. PZA reabsorption was reversibly decreased when lactate was added to the perfusate, indicating that it might occur through the sodium-lactate cotransport. The addition of PAH to the bath had a slight stimulatory effect on PZA reabsorption, suggesting a component of anion exchange in the overall PZA reabsorption. However, SITS added to either the perfusate or the bathing medium induced a non-significant decrease in PZA reabsorption, confirming the minor part of an anion exchange mechanism in this reabsorptive process. PZA reabsorption was not affected by the establishment of a bath-to-lumen H+ gradient, and was only moderately decreased after carbonic anhydrase inhibition by ethoxyzolamide, in opposition to what is known for the reabsorbed anion salicylate. The secretory transport of PZA was saturable and also dependent on a normal Na+/K+-ATPase activity. It is concluded that PZA is bidirectionally transported by facilitated mechanisms in the rabbit proximal S2 segment, one major reabsorptive mechanism appearing to be a sodium-anion cotransport, which might be the sodium-lactate reabsorbing mechanism.
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PMID:Pyrazinoate transport in the isolated perfused rabbit proximal tubule. 379 19

PAH transport and Na-K-ATPase activity markedly increase during the first month of postnatal life. Pretreatment of rats with PAH or cyclopenthiazide induces a stimulation of in vitro PAH accumulation in renal cortical slices, whereas Na-K-ATPase activity is unchanged in comparison to saline-pretreated controls. 5 mM ouabain in the incubation medium reduces PAH accumulation. Developmental pattern and stimulation effects are pronounced as in controls. The ouabain-insensitive component of net PAH accumulation progressively increases with age and is significantly enhanced following drug pretreatment, whereas the ouabain-sensitive component of net PAH accumulation shows relatively slight modifications. Consequently, Na-K-ATPase seems not to be linked with postnatal maturation or drug-induced stimulation in tubular PAH transport.
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PMID:p-Aminohippurate (PAH) transport and Na-K-ATPase activity in rat renal cortical slices during postnatal maturation and drug-induced stimulation. 631 68


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