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)

A) The proximal nephron and perinatal regulation of extracellular volume. 1. The glomerular capillary permeability coefficient (Kf) changes mainly because of an increasing capillary hydraulic conductance (Lp) within the autoregulatory range of renal perfusion pressure. 2. Proximal tubule hydrostatic hydraulic conductance and response to transmural protein concentration gradients is high during perinatal adaptation. 3. Proximal tubule paracellular shunt pathways are more important for absorption during differentiation than at maturity. 4. Basolateral membrane area of the single epithelial segment (10(-6) micron2 mm-1) increases and the typical basal labyrinth architecture develops. 5. The activity of the transport enzyme Na-K-ATPase increases in parallel to the basolateral membrane area to result in a constant number of enzyme sites during normal ontogeny. B) The distal nephron and perinatal regulation of extracellular osmotic activity. 6. Inner medullary urea content increases at osmotic equilibrium between interstitium and collecting duct. 7. The loop of Henle gradually dilutes the isotonic luminal fluid in the course of perinatal differentiation. 8. The thick ascending segment of the loop of Henle differentiates its anisotonic transport by increasing the Na-Chloride transport at constant hydraulic conductivity. 9. Ultrastructure and N-A-K-ATPase activity of the diluting segment (TAL) change greatly during ontogeny. 10. The centrifugal pattern of renal maturation from the juxtamedullary towards the superficial cortical layers leads to an intracortical profile of structure and function.
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PMID:Nephron function and perinatal homeostasis. 15 Feb 48

Previous studies have suggested the presence of an H(+)-K(+)-ATPase in rat cortical and medullary intercalated cells with similar properties to the gastric proton pump. The purpose of this study was to determine the functional contribution of an H(+)-K(+)-adenosinetriphosphatase(ATPase) to total CO2 (tCO2) transport along the rat collecting duct. After baseline determination of tCO2 transport in isolated perfused collecting duct segments, Sch 28080 (10 microM) was added to either the perfusate or bath. When Sch 28080 was added to the perfusate, there was no effect in the cortical collecting duct (CCD, 20.8 +/- 6.7 vs. 25.3 + 3.0 pmol.mm-1.min-1), but a marked decrease in tCO2 absorption was effected in both the outer medullary (OMCD, 37.6 + 6.2 vs. 10.7 +/- 4.1 pmol.mm-1.min-1) and initial inner medullary collecting duct (IMCD1, 34.4 +/- 8.1 vs. 16.2 +/- 5.6 pmol.mm-1.min-1). In the CCD from rats with acute alkalosis in vivo, Sch 28080 added to the bath inhibited tCO2 secretion in the CCD (-17.1 +/- 4.4 vs 3.5 + 3.3 pmol.mm-1.min-1). These findings suggest that 1) H(+)-K(+)-ATPase is important in tCO2 absorption in the OMCD and IMCD1 and in tCO2 secretion in the CCD, 2) HCO3(-)-absorbing intercalated cells differ functionally in the cortex and medulla, 3) HCO3- secretion is not the reverse process of HCO3- absorption in the CCD, and 4) H(+)-K(+)-ATPase is important in distal acidification under normal and altered acid-base conditions.
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PMID:H(+)-K(+)-ATPase activity in rat collecting duct segments. 131 8

1. In the nephrotic syndrome the kidneys retain salt and water, which leads to oedema formation. The site of this sodium retention has been localized in the cortical collecting tubule by micropuncture studies. Whether or not this phenomenon is an intrinsic renal problem or is the consequence of changes in hormonal activities is still a matter of discussion. 2. Using the model of puromycin aminonucleoside-induced nephrotic syndrome in the rat, we measured Na+,K(+)-ATPase activity in nephron segments from control and nephrotic rats and investigated the regulatory role of aldosterone and endogenous-ouabain-displacing factor. 3. Nephrotic animals had a twofold increase in Na+,K(+)-ATPase activity in the cortical collecting tubule only (control versus nephrotic: 1065 +/- 68 versus 2081 +/- 274 pmol h-1 mm-1, P = 0.036), which was not modified by adrenalectomy and was independent of the kidney content of endogenous ouabain-displacing factor. Na+,K(+)-ATPase activity in the cortical collecting tubule correlated with the sodium balance in both control and nephrotic rats. 4. The data are consistent with the view that sodium retention in this model of the nephrotic syndrome is a primary event, i.e. an increase in sodium transport throughout the cortical collecting tubule expressed as a twofold increase in Na+,K(+)-ATPase activity which is no longer under hormonal regulation (aldosterone and endogenous ouabain-displacing factor).
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PMID:Na+,K(+)-ATPase activity and hormones in single nephron segments from nephrotic rats. 164 23

Dopamine exerts numerous actions on the kidney but the precise location of its receptor subtypes along the nephron is unknown. Using a microassay we determined the specific binding of 125I-Sch 23982, a specific and selective dopamine-1 (DA1) receptor antagonist, to microdissected glomeruli and tubule segments. Binding of 125I-Sch 23982 in the proximal convoluted tubule (PCT) was time- and concentration dependent, saturable and reversible. The linear Scatchard plot of saturation experiments suggested binding to a single site with an apparent Kd of 16.7 nM and Bmax of 0.4 fmol.mm-1 in the PCT, and 6.2 nM and 0.1 fmol.mm-1 in the cortical collecting tubule (CCT). Mapping of DA1 binding sites along the nephron revealed their presence in each of the segments examined, albeit in markedly different concentrations: the highest specific binding was measured in PCT followed by the pars recta. Binding was less in the distal nephron, and least in the medullary and cortical thick ascending limb. Modest binding was also detected in glomeruli. In cortical collecting tubules competition studies with unlabeled dopamine and probes for DA1 (Sch 23390, fenoldopam), DA2 (domperidone, S-sulpiride), serotonergic (serotonin, ketanserin, mianserin), and alpha-(phentolamine) and beta-(propranolol) adrenergic receptors indicated a rank-order potency for displacement of 125I-Sch 23982 binding, consistent with labeling of DA1 receptors. Dopamine inhibited Na/K-ATPase both in PCT and CCT, an effect duplicated in the latter segment by the DA1 agonist fenoldopam, and blocked by the DA1 antagonist Sch23390.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization of dopamine-1 receptors along the microdissected rat nephron. 166 May 93

The present study was designed to quantitate the amount and to map the localization of N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) activity in microdissected segments of the rat nephron. After complete nephron mapping the effect of chronic metabolic acidosis and alkalosis on enzyme activity was determined. In control animals the highest enzyme activity was found in the early proximal convoluted tubule of juxtamedullary nephrons; superficial early proximal tubule as well as medullary and cortical thick ascending limbs and collecting ducts also contained substantial activity. Enzyme activity in the papillary collecting duct before entry into the ducts of Bellini was 329 +/- 93 pmol.mm-1.h-1 (n = 8); after entry, however, enzyme activity was approximately one-fourth that value (60 +/- 9 pmol.mm-1.h-1, n = 8, P less than 0.01). No NEM-sensitive ATPase activity was found in the thin limbs of the loop of Henle. Enzyme activity increased in both the medullary and cortical thick ascending limbs as well as in the cortical collecting tubule in response to NH4Cl-induced chronic metabolic acidosis; in the cortical collecting duct, metabolic acidosis increased maximum activity (Vmax) but did not change Michaelis-Menten constant (Km). In the proximal convoluted tubule, enzyme activity decreased with metabolic acidosis. Bicarbonate loading had no effect on enzyme activity except in the most distal portion of the collecting duct where it was stimulated. These results show that NEM-sensitive ATPase activity exists throughout much of the rat nephron. These data suggest that both the cortical collecting tubule and thick ascending limb are regulatory sites of distal urinary acidification during acid loading.
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PMID:NEM-sensitive ATPase activity in rat nephron: effect of metabolic acidosis and alkalosis. 213 83

Glucose absorption was investigated in isolated perfused proximal straight tubules from rats by use of a newly developed ultramicrofluorometric assay. This assay takes advantage of the increase in fluorescence associated with the reduction of NAD to NADH while glucose is degraded to 6-phosphogluconate. When tubules were perfused at 6.70 +/- 0.42 nl.mm-1.min-1, the mean rate of glucose absorption was 11.0 +/- 1.0 pmol.mm-1.min-1, and the mean rate of fluid absorption was 0.61 +/- 0.06 nl.mm-1.min-1. Glucose transport is generally due to Na-glucose cotransport in the proximal nephron. In the rat proximal straight tubule, glucose absorption also appeared to be primarily due to Na-glucose cotransport, since 10(-4) M phlorizin inhibited absorption by 100%, as did inhibition of Na(+)-K(+)-ATPase by K removal. To determine the maximum rate of transport, tubules were perfused at rates greater than 20 nl.mm-1.min-1 with a solution containing 5.5 mM glucose. The maximum rate of glucose absorption was approximately 20 pmol.mm-1.min-1 under these conditions. The concentration of glucose that supports 50% of the maximum rate of absorption, Km, was 0.6 mM. When tubules were perfused at flow rates of less than or equal to 2 nl.mm-1.min-1, the luminal glucose concentration reached a limiting value of 0.47 mM with 5.5 mM glucose in the bath. The glucose permeability was 3.1 X 10(-6) cm/s.
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PMID:Glucose absorption by isolated perfused rat proximal straight tubules. 222 Oct 96

To study proximal tubule bicarbonate absorption that is not due to the neutral Na+-H+ antiporter, mid to late proximal convolutions of the rat kidney were microperfused in vivo with a sodium-free choline solution containing 10(-3) M amiloride. The average sodium concentration resulting from sodium influx was 12 mM. At such low intraluminal [Na+], 10(-3) M amiloride should have inhibited the Na+-H+ antiporter by greater than 95%. When 25 mM HCO3- was in the perfusion fluid, measured total CO2 absorption was 100 pmol.mm-1.min-1. When luminal [HCO3-] was raised to 50 mM, and blood [HCO3-] was also raised to approximately 50 mM to avoid a transepithelial HCO3- concentration gradient, total CO2 absorption increased to greater than 300 pmol.mm-1.min-1. Thus raising intraluminal HCO3- concentration caused a marked increase in total CO2 absorption even though intraluminal [Na+] was low and amiloride was present. Control perfusions containing 140 mM Na+ yielded total CO2 absorption that was approximately 100 pmol.mm-1.min-1 higher than with the respective sodium-free perfusion solutions. In additional experiments, either DCCD or NEM was added to sodium-free perfusion solutions to inhibit H+-ATPase. These inhibitors reduced Na+-H+ independent total CO2 absorption markedly. Our observations suggest that under physiological acid-base conditions, sodium-independent H+ secretion can account for approximately 50% of total HCO3- absorption in mid to late proximal convolutions. This mechanism is stimulated by an increase in ambient HCO(-3) concentration to a degree that might account for the load-dependency of proximal HCO(-3) absorption in these segments of the proximal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proximal bicarbonate absorption independent of Na+-H+ exchange: effect of bicarbonate load. 253 46

We examined the hypothesis that proton-potassium-activated adenosine triphosphatase (H-K-ATPase) mediates K absorption and acidification in the inner stripe of the outer medullary collecting duct (OMCDi). Rabbits were fed a low-K diet (0.55% K) for 7-14 d because we have demonstrated previously that this low-K diet stimulates K-absorptive flux by the OMCDi. Proton secretion was measured as net total CO2 flux (JTCO2) by microcalorimetry. After basal collections, either vehicle or an inhibitor of gastric H-K-ATPase, omeprazole (0.1 mM), was added to the perfusate during the second period. Addition of vehicle to the perfusate changed neither the transepithelial voltage (VT, in millivolts) nor the JTCO2. In contrast, the addition of omeprazole (0.1 mM) to the perfusate abolished JTCO2 (from 14.5 +/- 5.6 to -0.1 +/- 3.1 pmol.mm-1.min-1) without significantly affecting VT. In additional experiments, in 16 tubules there was significant net K absorption (JK) of 5.0 +/- 1.0 pmol.mm-1.min-1 during the basal period, which exceeded the rate of K absorption that could be attributed to a paracellular voltage-mediated pathway (JKP = 1.0 +/- 0.4 pmol.mm-1.min-1, P less than 0.01). Administration of vehicle did not significantly affect either VT or JK. However, omeprazole abolished JK (from 5.1 +/- 1.0 to 0.1 +/- 2.5 pmol.mm-1.min-1) without affecting VT or JNa. The present results demonstrate that the OMCDi possesses an active, omeprazole-sensitive acidification and K-absorptive mechanism. These findings are consistent with the presence of H-K-ATPase activity in this nephron segment.
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PMID:Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase. 254 29

Morphological studies have demonstrated that a chronic increase in distal Na+ delivery causes hypertrophy of the distal convoluted tubule (DCT). To examine whether high NaCl-intake also causes functional changes in the well defined DCT, we measured transmural voltage (VT), lumen-to-bath Na+ flux (JNa(LB], and net K+ secretion (JK(net] in DCTs obtained from control rabbits and those on high NaCl-intake diets. The lumen negative VT was significantly greater in the high NaCl group than in the control group. The net K+ secretion (pmol mm-1 min-1) was greater in the high NaCl-intake group (54.1 +/- 13.0 vs 14.7 +/- 5.6). The K+ permeabilities in both luminal and basolateral DCT membranes, as assessed by the K+-induced transepithelial voltage deflection inhibitable with Ba2+, were increased in the experimental group. The lumen-to-bath 22Na flux (pmol mm-1 min-1) was also greater in the experimental group (726 +/- 119 vs 396 +/- 65). The VT component inhibitable with amiloride was also elevated in the high NaCl-intake group. Furthermore, Na+-K+-ATPase activity of the DCT was higher in the experimental than in the control group. We conclude that high NaCl intake increases both Na+ reabsorption and K+ secretion by the DCT. This phenomenon is associated with an increased Na+-K+-ATPase activity along with increased Na+ and K+ permeabilities of the luminal membrane, and an increase in the K+ permeability of the basolateral membrane. Cellular mechanisms underlying these functional changes remain to be established.
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PMID:Effect of high NaCl intake on Na+ and K+ transport in the rabbit distal convoluted tubule. 255 Aug 87

A plasma membrane ATPase sensitive to inhibition by N-ethylmaleimide (NEM) and insensitive to inhibition by oligomycin and ouabain has been shown to be involved in acidification of urine in the turtle bladder. The activity of this NEM-sensitive ATPase was determined in four types of distal nephron segments of normal rats and in rats treated with ammonium chloride. The enzyme activity was determined by a fluorometric micromethod in which ATP hydrolysis was coupled to NADH oxidation. Significant activities (10-35 pmol ADP X min-1 X mm-1) of NEM-sensitive ATPase were present in the distal convoluted tubule (DCT) and in the cortical and outer and inner medullary collecting duct segments of normal rats. In metabolic acidosis produced by ammonium chloride treatment (plasma CO2 content = 15.3 +/- 0.8 mequiv./L), the NEM-sensitive ATPase activity was increased significantly (60-100%) in the collecting duct segments without showing a significant change in the enzyme activity in the DCT. Our data are consistent with the hypothesis that a plasma membrane H+-ATPase (inhibited by NEM but not by oligomycin or ouabain) is involved in H+ secretion in the mammalian collecting duct.
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PMID:Stimulation of an N-ethylmaleimide-sensitive ATPase in the collecting duct segments of the rat nephron by metabolic acidosis. 293 19


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