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)

Luminal brush border and contraluminal basal-lateral segments of the plasma membrane from the same kidney cortex were prepared. The brush border membrane preparation was enriched in trehalase and gamma-glutamyltranspeptidase, whereas the basal-lateral membrane preparation was enriched in (Na+ + K+1)-ATPase. However, the specific activity of (Na+ + K+)-ATPase in brush border membranes also increased relative to that in the crude plasma membrane fraction, suggesting that (Na+ + K+)-ATPase may be an intrinsic constituent of the renal brush border membrane in addition to being prevalent in the basal-lateral membrane. Adenylate cyclase had the same distribution pattern as (Na+ + K+)-ATPase, i.e. higher specific activity in basal-lateral membranes and present in brush border membranes. Adenylate cyclase in both membrane preparations was stimulated by parathyroid hormone, calcitonin, epinephrine, prostaglandins and 5'-guanylylimidodiphosphate. When the agonists were used in combination enhancements were additive. In contrast to the distribution of adenylate cyclase, guanylate cyclase was found in the cytosol and in basal-lateral membranes with a maximal specific activity (NaN3 plus Triton X-100) 10-fold that in brush border membranes. ATP enhanced guanylate cyclase activity only in basal-lateral membranes. It is proposed that guanylate cyclase, in addition to (Na+ + K+)-ATPase, be used as an enzyme "marker" for the renal basal-lateral membrane.
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PMID:Preparation of renal cortex basal-lateral and bursh border membranes. Localization of adenylate cyclase and guanylate cyclase activities. 1 97

The effects of deoxycholate, taurocholate and cholate on transport and mucosal ATPase activity have been investigated in the rat jejunum in vivo using closed-loop and perfusion techniques. In the closed-loops, 5 mM deoxycholate selectively inactivated (Na+ + K+)-ATPase, and net secretion of Na+ induced by 2.5 mM deoxycholate was due to reduced lumen to plasma flux of the ion; deoxycholate (2.5 mM) produced marked inhibition of 3-0-methylglucose transport. Luminal disappearance rates of deoxycholate (60.5 plus or minus 2.9% per g wet st of gut) greatly exceeded those of taurocholate (4.3 plus or minus 1.0). In the perfusion studies 1 mM deoxycholate induced net secretion of water, Na+ and C1-, and inhibited active glucose transport; concomitantly "total" ATPase, (Na+ + K+)-ATPase, and Mg-2+-ATPase were inhibited. At higher concentrations (5 mM) deoxycholate stimulated Mg-2+-ATPase activity. Taurocholate and cholate at 1mM had no effect on transport of (Na+ + K+)-ATPase. Mucosal lactase, sucrase and maltase activities were not affected by 1 mM deoxycholate, taurocholate or cholate. These results suggest that deoxycholate inhibits sodium-coupled glucose transport by inhibition of (Na+ + K+)-ATPase at the lateral and basal membranes of the epithelial cell, rather than from an effect at the brush-border membrane level.
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PMID:A comparative study on the effects of different bile salts on mucosal ATPase and transport in the rat jejunum in vivo. 12 87

Luminal (brush border) and antiluminal (basal-lateral) membranes were isolated from canine renal cortex. The enzyme marker for luminal membrane, alkaline phosphatase was enhanced 19-fold and the antiluminal enzyme marker, (Na+ + K+)-ATPase, was enhanced 22-fold in their respective membrane preparation, while the amount of cross contamination was minimal. Contamination of these preparations by enzyme markers for lysosomes, endoplasmic reticulum and mitochondria was also low. Routinely, more than 50 mg membrane protein was isolated for each membrane. Electron micrographs showed that the membranes were uniform in size, appearance, and vesicular in nature. An examination of the orientation of these membranes showed that 76.5% of the antiluminal membranes and 86% of the luminal membranes were right-side out.
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PMID:Isolation of luminal and antiluminal membranes from dog kidney cortex. 22 Oct 18

Previous studies suggest that enhancement of rubidium tracer (86Rb) lumen-to-bath efflux following removal of luminal Na is mediated in part by a Ba-insensitive pathway. To determine the role of a primary active K pump in this response, we examined the action of known inhibitors of H-K-ATPase (Sch 28080) and Na-K-ATPase (ouabain) on the 86Rb lumen-to-bath efflux coefficient (KRb). Luminal Sch 28080 (10 microM) significantly reduced KRb by 39 +/- 8.0% (P less than 0.05), whereas luminal ouabain (0.1 mM) reduced KRb by 10 +/- 14% (P = not significant), suggesting that a luminal H-K-ATPase mediates Rb efflux. To examine whether H-K-ATPase mediates Rb in KRb following removal of luminal Na, additional experiments were conducted to examine the effect of Sch 28080 on KRb in the presence and the absence of luminal Na. In the presence of luminal Na, 10 microM Sch 28080 reduced KRb by 15 +/- 5.0%. However, in the absence of luminal Na, 10 microM Sch 28080 decreased KRb by 48 +/- 8.2%. The percentage inhibition of KRb by Sch 28080 was significantly greater in the absence of luminal Na than in its presence (P less than 0.01), suggesting that the enhancement of KRb following removal of luminal Na is mediated in part by an H-K-ATPase pathway. In either case transepithelial voltage was not significantly altered. In contrast to the lack of effect of luminal ouabain, addition of 0.1 mM ouabain to the bath increased KRb (69.8 +/- 11.1 vs. 95.9 +/- 18.7 nm/s, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:H-K-ATPase enhancement of Rb efflux by cortical collecting duct. 132 55

To examine the pathways of K permeation in the cortical collecting duct (CCD) from K-restricted rabbits, we studied the effects of the following three maneuvers: 1) luminal amiloride addition; 2) luminal Ba addition; and 3) luminal Na removal. Luminal addition of amiloride (1 mM) significantly increased the 86Rb lumen-to-bath efflux coefficient (KRb), and this effect was fully blocked by the presence of 2 mM luminal Ba. Addition of 2 mM luminal Ba reduced KRb both in the absence of luminal Na and in the presence of luminal Na. In contrast to the effect of amiloride addition, removal of luminal Na significantly increased KRb, but neither 2 mM luminal Ba nor 4 mM luminal Ba totally abolished this effect. However, simultaneous addition of luminal Ba and Sch 28080 (10 microM) fully inhibited the increase in KRb upon luminal Na removal, indicating that luminal Na removal enhances Rb efflux in part via H-K-adenosinetriphosphatase (H-K-ATPase). To test whether Na acts as a partial agonist for cation efflux via the H-K-ATPase we examined the effect of Sch 28080 on the 22Na lumen-to-bath efflux coefficient (KNa). These studies were conducted in the presence of 0.1 mM luminal amiloride to block fully apical conductive Na efflux, and the effect of Sch 28080 on KNa was examined at two different ambient K concentrations. In the presence of 0.5 mM K, Sch 28080 (10 microM) significantly inhibited KNa from 47.6 +/- 4.8 to 35.0 +/- 6.8 nm/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of rubidium permeation by rabbit cortical collecting duct during potassium restriction. 133 11

The rat MTAL secretes protons into the tubular fluid and thus absorbs bicarbonate at substantial rates. Yet the cellular mechanisms of H+/HCO3- transport in the rat MTAL remain largely unsettled. We have performed intracellular pH recovery studies with use of the fluorescent probe BCECF in suspensions of rat MTAL fragments. Luminal H+ secretion occurs by two mechanisms (each responsible for 50% of the normal pHi recovery rate): (1) an electroneutral Na+/H+ antiporter that has an Na-Km of about 11 mM and is inhibited by amiloride (Ki = 2.8 x 10(-5) M); (2) a primary H+ pump that is inhibited by 10(-4) M NEM and 10(-4) M omeprazole, but not by 10(-4) M vanadate or removal of external K. These results suggest the presence of a vacuolar H(+)-ATPase rather than a H(+)-K(+)-ATPase. Basolateral HCO3 exit occurs predominantly by a Cl(-)- and Na(+)-independent electroneutral K+/HCO3- symporter, that has an HCO3-Km of about 17 mM, and is partially inhibited by 10(-4) M DIDS. Basolateral HCO3- efflux was not accompanied by variations of membrane potential monitored with the Em-sensitive fluorescent probe DIS-C3-5, and was not affected by maneuvers that depolarize the cells. It was strongly inhibited by cellular K depletion and dependent on transmembrane K gradient. We conclude that the rat MTAL should secrete protons through both Na+/H+ antiporter and H(+)-ATPase, and that basolateral HCO3- exit should occur through an electroneutral K+/HCO3- symporter.
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PMID:Mechanisms of H+/HCO3- transport in the medullary thick ascending limb of rat kidney. 165 72

To examine mechanisms of H+ extrusion in the inner stripe of outer medullary collecting duct (OMCDIS), cell pH (pHi) was measured microfluorometrically in in vitro perfused tubules by use of 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In total absence of luminal and peritubular Na+, pHi recovery from an acid load (NH3/NH+4 pulse) occurred at an initial rate of 0.13 +/- 0.02 pH units/min, whereas in the presence of 135 mM peritubular Na+, pHi recovered at 1.40 +/- 0.28 pH units/min. Na(+)-dependent pHi recovery was completely inhibited by 1.0 mM peritubular amiloride. Luminal Na+ (135 mM) addition had no effect on pHi recovery. Na(+)-independent pHi recovery from acid load was manifest by a triphasic response: 1) initial slow alkalinization; 2) slow cell acidification; and 3) a final phase that exhibited gradually increasing rates of alkalinization, returning pHi above the initial control level (pre-NH3/NH+4 pulse). Luminal N-ethylmaleimide (NEM, 500 microM), an H(+)-ATPase inhibitor, significantly inhibited initial rate of pHi recovery and total pHi recovery; whereas 500 microM peritubular NEM had no effect on initial rate of pHi recovery. Luminal SCH 28080 (100 microM), an H(+)-K(+)-ATPase inhibitor, had no effect on initial rate of pHi recovery or total pHi recovery. Thus rabbit OMCDIS possesses both an apical membrane NEM-sensitive, SCH 28080-insensitive, Na(+)-independent H+ extrusion mechanism (likely a simple H(+)-translocating ATPase) and a basolateral membrane amiloride-sensitive Na(+)-H+ antiporter.
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PMID:Apical and basolateral membrane H+ extrusion mechanisms in inner stripe of rabbit outer medullary collecting duct. 217 59

In brush border membrane vesicles prepared from mammalian kidney cortex, amiloride is a potent inhibitor of the Na+/H+ exchanger. In the present study, in vivo microperfusion was used to examine the effect of luminal amiloride on transport in the rat superficial proximal convoluted tubule. At a perfusion rate of 14 nl/min, addition of 10(-3) M amiloride to artificial early proximal tubular fluid reduced bicarbonate absorption from 103 +/- 7 to 81 +/- 5 pmol mm-1 X min-1 and volume absorption from 2.03 +/- 0.15 to 1.57 +/- 0.06 nl X mm-1 X min-1. Glucose efflux was unchanged, excluding nonspecific inhibition of Na+-K+-ATPase. Luminal amiloride at 10(-4) M did not affect bicarbonate absorption or volume absorption. At a perfusion rate of 41 nl/min, 10(-3) M amiloride reduced bicarbonate absorption from 179 +/- 8 to 114 +/- 9 pmol X mm-1 X min-1, a significantly greater inhibition than that seen in tubules perfused at 14 nl/min. Amiloride at 10(-3) M had no significant effect on sodium chloride absorption as measured by volume flux from an artificial late proximal tubular fluid. The results show that luminal amiloride specifically inhibits proximal acidification and demonstrate involvement of the Na+/H+ antiporter in proximal tubular acidification. However, the inhibition of acidification is less than the inhibition of Na+/H+ exchange predicted by vesicle studies.
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PMID:Amiloride inhibition of proximal tubular acidification. 298 47

Isolated perfused medullary thick ascending limbs from rabbits were studied to determine the mechanism of ammonium ion absorption. Under control conditions, thick ascending limbs spontaneously absorbed NH4+ and generated a lumen-positive potential. When these tubules were chemically voltage clamped to lumen-negative potentials by lowering the bath NaCl concentration, NH4+ absorption persisted. Thus NH4+ was absorbed against an electrochemical gradient. The active flux accounts for most of the net flux under control conditions, the remainder being due to passive paracellular NH4+ diffusion. The NH4+ permeability, measured in separate experiments, was high (1.50 +/- 0.25 x 10(-4) cm/s) compared with values in other segments. The NH3 permeability was relatively low (3.1 +/- 0.5 x 10(-3) cm/s). Luminal furosemide (10(-4) M) eliminated most of the active NH4+ flux, indicating that a major fraction of the active flux is dependent on apical entry of NH4+ via the Na+ -K+ -2Cl- cotransporter (presumably by substitution for K+). The remaining active flux was completely inhibited by 10(-4) M ouabain in the bath. Active chloride absorption was maintained when NH4+ entirely replaced K+ in bath and perfusate, indicating that NH4+ substitutes for K+ on the apical cotransporter and the basolateral Na+ -K+ -ATPase. Ammonium absorption provides an active "single effect" for countercurrent multiplication of NH4+ in the renal medulla.
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PMID:Active NH4+ absorption by the thick ascending limb. 339 13

Inhibition of basolateral Na+/K+ ATPase by ouabain eventually abolishes transport of glucose. The present study was performed to test, if this effect is due to a dissipation of the electrochemical gradient for sodium or due to a regulatory inhibition of sodium-coupled glucose entry across the luminal membrane at increasing intracellular sodium activity. To this end, proximal convoluted tubules of the doubly perfused isolated frog kidney were perfused alternatively with solutions containing either 5 mmol/l glucose or raffinose. The potential difference across the peritubular cell membrane (PDpt) and across the epithelium (PDte) has been recorded with conventional and across the peritubular cell membrane with ion selective microelectrodes (PDpt). In the absence of luminal glucose PDpt is (+/- SEM) -54.0 +/- 2.4 mV, PDte = -1.2 +/- 2.0 mV and PDNapt = -96 +/- 5 mV. The electrochemical gradient for sodium (mu Na+) amounts to 95 mV and intracellular sodium activity to 14 mmol/l (extracellular sodium activity is 74 mmol/l). Luminal application of glucose leads to a rapid depolarisation of PDpt (delta PDpt = 8.6 +/- 0.9 mV and PDNapt (delta PDNapt = 11.1 +/- 3.0 mV) and to hyperpolarisation of PDte (delta PDte = -0.8 +/- 0.2 mV). The peritubular application of ouabain leads to a gradual, reversible and proportional decline of PDpt, PDNapt and mu Na+. Glucose induced delta PDpt and delta PDNapt decrease in parallel to PDpt and PDNapt, resp. In a separate series, the lumped conductance (Gm) of the luminal and basolateral cell membrane has been determined, which amounts to 2.4 +/- 0.3 microS/mm (tubule length). Gm decreases 23 +/- 4%, when PDpt is decreased to half.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of intracellular sodium activity on the transport of glucose in proximal tubule of frog kidney. 608 87


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