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)

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

This study utilized electron microscopy and enzyme histochemistry to examine the morphological steps associated with the formation of a lumen in the end-buds of the embryonic rat submandibular gland. Lumen formation involved the development of junctional complexes by the central cells of the end-buds late on the 16th day of gestation. These junctional complexes established the apical domains of the presecretory cells, and cytofilament aggregates were observed beneath the presumptive luminal plasma membranes. This central area of the end-buds showed strong myosin ATPase activity, presumably associated with the cytofilaments. On the 17th day of gestation, small lumina appeared at the sites delineated by the junctional complexes. The myosin ATPase activity appeared to surround the newly opened lumina. By the 18th day of gestation, microvilli were seen projecting into the lumina, and secretory granules were often visible in the apical cytoplasm near the luminal plasma membranes of the early secretory cells. Myosin ATPase activity was greatly reduced once the lumina had formed.
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PMID:Lumen formation during development of the rat submandibular gland. 347 54

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

Transepithelial (psi T) and basolateral (psi BL) potential difference was measured in rabbit proximal convoluted tubules perfused in vitro. In control solution without protein, the mean psi BL was -54 +/- 2.2 mV (n = 57). Luminal substitution of K by Na had no effect. Complete luminal substitution of glucose and alanine, 110 mM substitution of Na or NaCl produced transient hyperpolarizations of psi BL of 14, 10, and 13 mV, respectively, with a return close to the control value within 4-8 min in all cases. Returning to control solution produced similar time-course transient depolarizations of psi BL of 17, 11, and 16 mV, respectively, again with a return to the control value in 4-10 min. Omission of glucose and alanine in the perfusate produced a decrease in cell volume of 14% that was maximal in 4 min with a complete recovery in the post-control period. A 110 mM luminal or peritubular substitution of Cl by cyclamate produced no significant effect on psi BL after taking into account the large psi T generated by the diffusion of Cl across the paracellular pathway. On the other hand, complete peritubular substitution of K by Na and 110 mM substitution of Na or NaCl produced sustained but reversible depolarizations of psi BL of 37.5, 10.2, and 20.4 mV, respectively. The transient nature of the hyperpolarization following luminal substitution of glucose, alanine, or Na can be interpreted in terms of changes in the intracellular sodium activity that would affect the Na-K-ATPase pump. Similarly, the sustained depolarization seen after a peritubular substitution of K and Na would also be compatible with a decrease in the basolateral ionic pump activity.
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PMID:Luminal and peritubular ionic substitutions and intracellular potential of the rabbit proximal convoluted tubule. 620 98

The effects of Triton WR-1339 and phenobarbital on ethinyl estradiol bile secretory failure were examined to determine the mechanism responsible for decreased bile salt excretion. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored bile salt independent bile flow and maximum taurocholate transport, whereas phenobarbital corrected bile flow only. Ethinyl estradiol decreased the activities of Na(+)-K(+)-ATPase, 5'-nucleotidase, while increasing the activities of Mg(++)-ATPase and alkaline phosphatase. In contrast to these heterogeneous changes in surface membrane enzyme activities, the number and affinity of [(14)C]cholic acid carriers were not altered. When administered in vivo or added directly to surface membrane fractions Triton WR-1339 restored the activities of Na(+)-K(+)-ATPase and Mg(++)-ATPase of rats treated with ethinyl estradiol through a process that did not require protein synthesis (unaffected by cycloheximide). Phenobarbital also restored the activity of Na(+)-K(+)-ATPase to control levels, but, unlike Triton WR-1339 it did not correct the defect responsible for reduced bile salt secretion. Ethinyl estradiol increased the concentration of cholesterol esters in surface membrane fractions. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored cholesterol ester concentrations to normal, whereas phenobarbital did not. These combined data suggest that decreased or altered bile salt carriers or reduced sodium driving forces resulting from impaired activity of Na(+)-K(+)-ATPase are not responsible for decreased bile salt excretion in ethinyl estradiol-treated rats. It is proposed that the diverse changes in surface membrane function, which are associated with ethinyl estradiol bile secretory failure, may be the result of a generalized alteration in membrane lipid structure.
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PMID:Reversal of ethinyl estradiol-induced bile secretory failure with Triton WR-1339. 624 35

The effect of vanadate, a potent inhibitor of Na-K-ATPase, on the hydroosmotic response to vasopressin (AVP) and transepithelial voltage (Vt) in cortical collecting tubules was examined. At 37 degrees C, exposure of collecting tubules to bath vanadate (10(-4) M) for 30 min inhibited the increase in hydraulic water permeability (Lp) in response to AVP or 8-bromo-cyclic adenosine monophosphate by 68 and 76%, respectively. When vanadate was present only in the lumen no inhibition of the AVP response was observed. Incubation of tubules with ouabain (10(-5) M) for 30 min inhibited the AVP-induced increase in Lp to the same extent as vanadate. At 25 degrees C, vanadate inhibited the increase in Lp by AVP if added before but not after the hormone. Addition of vanadate to the bath caused a rapid decrease in the lumen-negative Vt that is consistent with Na-K-ATPase inhibition. Luminal vanadate also inhibited Vt but the rate of decrease of Vt was much slower than in the presence of bath vanadate. We conclude that vanadate inhibits the development but not the maintenance of the AVP-induced increase in water permeability in the collecting tubule. Since the effect of ouabain was similar to that of vanadate, the results suggest that inhibition of Na-K-ATPase directly or indirectly interferes with the initiation of the AVP-induced increase in luminal membrane water permeability at a site distal to cAMP formation.
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PMID:Inhibition of vasopressin action by vanadate in the cortical collecting tubule. 655 36

Although oral contraceptives (OCs) are yet to be legalized in Japan, it is estimated that at least 500,000 women were on pills in 1975. Intrahepatic cholestasis has been associated with OC in the Western countries, but only a few cases have been reported in Japan. A case of pill-related intrahepatic cholestasis in a 25-year old housewife will be presented in terms of clinical/pathological findings, changes in plasma and bile acid levels, and the effect of phenobarbital on bile stagnation. The patient had been taking 1 pill (Anovlar)/day, 25 days a month, for 5 months, and had experienced exhaustion, nausea, and constipation after 3 months of use; body itch and jaundice symptoms after 4 months. Cholangiography showed neither enlargement of the bile duct nor obstruction of the bile duct outside the liver. The condition was diagnosed as pill-related intrahepatic cholestasis. Total bilirubin was considerably raised; serum transaminase was moderately raised. Electromicroscopy showed the enlargement of bile canaliculi, which had electron dense bile content. Hepatic cellular peroxisome significantly increased. Plasma bile acid level, which was slightly raised initially, came down to the normal range when total bilirubin was back to normal with daily administration of phenobarbital 2 mg/kg. Studies which included experiments with rats as well as clinical-pathological results mentioned above suggested that bile stagnation was caused by ethinyl estradiol. By lowering bile canaliculi Na-K ATPase activity, ethinyl estradiol decreased bile acid independent of bile flow. Phenobarbital was effective for cholestasis by increasing bile canaliculi Na-K ATPase activity.
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PMID:[Intrahepatic cholestasis caused by oral contraceptives]. 714 55

In the absence of transepithelial electrochemical gradients, the direction of net K transport across the turtle urinary bladder is from the mucosal (M) to the serosal (S) solution. Under control conditions, M leads to S flux was 101 +/- 5 nmol . h-1 . (8 cm2)-1, S leads to M flux was 59 +/- 4, and the net absorptive flux was 42 +/- 6. The K absorptive pump was characterized by examining its dependence on voltage and ambient sodium and its sensitivity to mucosal ouabain. Lumen-negative voltages caused an increase rather than the expected decrease in active K absorption. Thus, the active K flux appeared to be coupled to a flow of positive charge in the opposite direction, possibly representing Na secretion in excess of K absorption. Net K absorption was abolished by removal of Na from the medium and by mucosal, but not serosal, addition of ouabain. The reverse electrogenicity, Na dependence, and ouabain sensitivity of K absorption indicate that the K pump of the mucosal membrane has characteristics of a Na-K-ATPase.
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PMID:Potassium absorptive pump at the luminal membrane of turtle urinary bladder. 728 30


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