Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Initial segments of the inner medullary collecting duct of the rat were perfused in vitro, and the electrophysiological properties of the apical and basolateral membranes were examined with KCl-filled microelectrodes. The fractional resistance of the apical membrane (FRa = Ra/Ra + Rbl) and the transepithelial resistance (RT) were estimated by cable analysis. In control tubules the transepithelial voltage (VT) averaged -2.2 mV, and the voltage across the basolateral membrane (Vbl) averaged -51.1 mV. RT was 11.9 k omega.cm (72.8 omega.cm2), and FRa was 0.94. Pretreatment of the rats with deoxycorticosterone (DOC)-pivalate for 7-10 days did not alter these electrophysiological properties. In control tubules, amiloride in the lumen (10(-5) M) changed VT from -3.0 to +1.4 mV and increased Vbl from -49.4 to -53.8 mV, RT from 12.5 to 13.6 k omega.cm, and FRa from 0.92 to 0.98. Thus the apical membrane is conductive to Na+. An increase of the bath K+ concentration from 4 to 15 mM caused an 18.8 mV depolarization of Vbl: barium in the bath also depolarized Vbl. A fivefold decrease in the [HCO3-] in the bath depolarized Vbl by 13.1 mV. 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) blocked this depolarization. Thus the basolateral membrane is conductive to K+ and HCO3-. Experiments with ouabain revealed a Na+-K+-ATPase in the basolateral membrane. Taken together, the results support a model in which electrogenic Na+ absorption is driven by the Na+-K+-ATPase in the basolateral membrane, with passive movement of Na+ occurring through an amiloride-sensitive conductive pathway in the apical membrane.
 ...
PMID:Characterization of apical and basolateral membrane conductances of rat inner medullary collecting duct. 271 19

Confluent sheets formed from primary culture of avian salt gland secretory cells exhibit a short-circuit current (Isc) in response to cholinergic and beta-adrenergic stimulation [Lowy, R. J., D. C. Dawson, and S. A. Ernst. Am J. Physiol. 249 (Cell Physiol. 18): C41-C47, 1985]. To establish the ionic basis for the Isc, transmural fluxes of 22Na and 36Cl were measured. Under short-circuit conditions there was little net flux of either ion in the absence of agonists. Addition of carbachol elevated net serosal-to-mucosal Cl flux to 1.71 mu eq.h-1.cm-2, whereas a smaller increase to 0.85 mu eq.h-1.cm-2 occurred with isoproterenol. Neither agonist altered net Na flux. The stimulated Isc accounted for 70% of the net Cl flux induced by carbachol and nearly 100% of that induced by isoproterenol. Replacement of Cl by gluconate or Na by choline abolished (carbachol) or greatly reduced (isoproterenol) the Isc, which could be restored in a dose-dependent fashion by ion restitution. Active ion transport was preferentially inhibited by basal (vs. apical) addition of ouabain, furosemide, or barium. The results provide evidence that cholinergic and beta-adrenergic agonists elicit active transmural Cl secretion. They further suggest that transport is dependent on the Na+-K+-adenosine-triphosphatase, a Na-Cl cotransport process, and a basal K conductance, all features of a secondary active Cl secretory mechanism.
 ...
PMID:Mechanism of ion transport by avian salt gland primary cell cultures. 273 44

Intracellular recordings were made from rat striatal neurones in vitro. In the presence of intracellular caesium and extracellular tetraethylammonium chloride (TEA) (5 mM) and barium (3 mM), long-lasting plateau potentials developed followed by a prominent voltage independent hyperpolarization which lasted several seconds. A similar afterhyperpolarization was observed when calcium was replaced by barium. The afterhyperpolarization was reduced in a potassium free medium and reversibly abolished in a Na+-free solution or by cooling the slice to 21-24 degrees C. It was also irreversibly blocked by ouabain (50 microM). This hyperpolarization may therefore result from the activation of a Na+,K+-ATPase electrogenic pump.
 ...
PMID:A ouabain-sensitive hyperpolarization in rat striatal neurones in vitro. 281 90

The relationship between K and ammonia transport was investigated in the turtle bladder. At serosal pH 6.4, ammonia transport is preferentially from serosa to mucosa and is, at least in part, mediated by NH4+ transport. Since K and NH4+ share similar features such as permeability and stimulation of Na-K-ATPase, we studied the interaction of transport of these ions by the turtle bladder. Removal of K from the mucosal solution inhibited partially ammonia transport from serosa to mucosa and the inhibition was reversible by restoration of K. In contrast, removal of serosal K failed to inhibit ammonia transport. Since NH4+ can replace K in the activation of Na-K-ATPase in turtle bladder plasma membrane fraction with similar K, we examined the effect of ouabain on ammonia transport. Ouabain added to the serosal solution failed to inhibit ammonia transport thus, suggesting that the Na-K-ATPase is not required for ammonia entry into the cell. Methylammonium (a competitive inhibitor of NH4+ transport in other systems) decreased both ammonia transport and the observed increase in short circuit current elicited by NH4Cl addition to the serosal solution. This finding suggests that NH4+ and methylammonium are transported through a common pathway in the serosal side. Since the permeability of the serosal side to K and NH4+ is similar, we evaluated the effect of serosal depolarization and the effect of barium, an inhibitor of K channels, on ammonia transport. Serosal depolarization inhibited ammonia transport but barium did not affect ammonia flux.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Relationship of K and ammonia transport by the turtle bladder. 282 79

Recent studies of rabbit colon have indicated the presence of a vanadate-sensitive K+-dependent proton pump, suggesting the existence of an H+-K+-ATPase. The participation of such a mechanism for colonic K+ absorption in the rat has not been determined. To this purpose, we attempted to detect the presence of pH-linked mechanisms for K+ absorption in rat distal colon using 86Rb as a marker for K+. We found that Rb+ absorption in Na-Ringer directly correlated with the in vitro partial pressure of CO2 (PCO2) in aldosterone-stimulated but not in control rats. Similar studies performed using Na-free Ringer demonstrated that PCO2 markedly augmented Rb+ absorption in both control and aldosterone-stimulated rat colon. Rb+ absorption was inhibited by orthovanadate, SCH28080, and mucosal ouabain in Na-free Ringer, but there was no effect of omeprazole, furosemide, or bumetanide. Barium applied to the serosa was also effective in inhibiting Rb+ absorption, suggesting that Rb+ exit from the cell was conductive. These findings are consistent with the presence of an active K+ pump that is activated by pretreatment with aldosterone and increased in vitro PCO2 and that is inhibited by orthovanadate, SCH28080, and mucosal ouabain. The constellation of findings suggests that participation of an ATPase that is not typical of either Na+-K+-ATPase or H+-K+-ATPase.
 ...
PMID:Aldosterone and PCO2 enhance rubidium absorption in rat distal colon. 296 41

The messenger roles of cyclic AMP and the calcium ion in stimulus-secretion coupling are considered in the frog and bovine corneal epithelium, respectively. In the frog cornea, epinephrine stimulates net C1 transport by increasing cyclic AMP content. This stimulation is associated with a larger apical membrane C1 conductance and basolateral membrane ionic conductance. The response of the apical membrane conductance is thought to result from an increase in cyclic AMP content whereas the basolateral membrane ionic conductance increase is unrelated based on measurements of the effects of the calcium channel antagonist, diltiazem, and the beta agonist, isoproterenol, on the electrical parameters and cyclic AMP content. The basolateral membrane is essentially K permselective since the K channel blocker, Ba, depolarized the intracellular potential difference and increased the basolateral membrane resistance. Diltiazem had even larger effects on these parameters suggesting that this compound is a more effective inhibitor of K channel activity than barium. In broken cell preparations of bovine corneal epithelium, a high affinity form of Ca + Mg activated ATPase is present (Km = .06 microM for Ca) and is essentially of plasma membrane origin. This ATPase activation is at a Ca activity similar to the expected intracellular value and suggests that this activity is the enzymatic basis for net Ca transport.
 ...
PMID:Roles of cyclic AMP and Ca in epithelial ion transport across corneal epithelium: a review. 299 Aug 18

To clarify the cause of the stimulation of p-aminohippurate (PAH) accumulation in rat kidney cortical slices by barium, an experiment was carried out with basolateral membrane vesicles isolated from rat kidney cortex. The effect of barium on PAH uptake by the membrane vesicles was compared with that of verapamil which also stimulated PAH accumulation in the slices. The enzyme marker for basolateral membrane, (Na+ + K+)- ATPase, was enriched 15-fold and the brushborder enzyme marker, alkaline phosphatase, was 1.3-fold in our membrane preparation. Contamination in this preparation by lysosomes, mitochondria and cytosol was also low but that by endoplasmic reticulum was slightly high as judged by the enzyme markers. PAH uptake by the membrane vesicles possessed the usual characteristics, i.e., sodium-dependence and probenecid-sensitivity. PAH uptake by the membrane vesicles was enhanced by barium, but not by verapamil. On the other hand, barium did not affect tetraethylammonium (TEA) uptake by the vesicles, and verapamil strongly inhibited it. Manganese also stimulated PAH uptake to the same extent as did barium, but calcium and strontium did not affect the uptake. Barium did not act on sodium transport in the membrane vesicles. An 'anion-sensitively transported lipophilic cation', triphenylmethylphosphonium iodide (TPMP), uptake was depressed by barium. These results suggest that barium stimulates selectively PAH uptake in basolateral membrane vesicles. Its stimulatory action may contribute at least partly to an increase in PAH accumulation in rat kidney cortical slices by this ion and may prove useful in an analysis of the mechanism of PAH transport system in renal basolateral membranes.
 ...
PMID:Effect of barium ion on p-aminohippurate transport in basolateral membrane vesicles isolated from rat kidney cortex. 299 5

Potassium fluxes in a suspension of rabbit proximal tubules were monitored using a potassium-sensitive extracellular electrode. Ouabain (10(-4) M) and barium (5 mM) were used to selectively quantitate the potassium efflux pathway (105 +/- 5 nmol K+ X mg protein-1 X min-1) and the sodium pump-related potassium influx (108 +/- 7), respectively. These equal and opposite fluxes suggest that potassium accumulation in the cell occurs mainly through the sodium pump and that potassium efflux occurs mainly through barium-sensitive potassium channels. Thus the activity of the sodium pump (Na,K-ATPase) in the basolateral membrane of the proximal tubule is balanced by the efflux of potassium, presumably across the basolateral membrane, which has a high potassium permeability. In addition, the effect of valinomycin and other ionophores was examined on potassium fluxes and several metabolic parameters [oxygen consumption (QO2), ATP content]. The addition of valinomycin to the tubules produced a net efflux of potassium which was quantitatively equivalent to the efflux produced by the addition of ouabain. The valinomycin-induced efflux was mainly due to the activity of valinomycin as a mitochondrial uncoupler, which indirectly inhibited the sodium pump by allowing a rapid reduction of the intracellular ATP. Amphotericin, nystatin, and monensin all produced large net releases of intracellular potassium. The action of the ionophores could be localized to the plasma or mitochondrial membrane and classified into three groups, as follows: those which demonstrated full mitochondrial uncoupler activity (FCCP, valinomycin), those which had no uncoupler activity (amphotericin B, nystatin); and those which displayed partial uncoupler activity (monensin, nigericin).
 ...
PMID:Potassium transport in the rabbit renal proximal tubule: effects of barium, ouabain, valinomycin, and other ionophores. 303 6

In the rectal gland of the spiny dogfish (Squalus acanthias), chloride enters the cell via a cotransport system together with sodium and potassium in a 2 Cl-: 1 Na+: 1 K+ stoichiometry. The system is energized by the electrochemical potential for sodium directed into the cell. Sodium is extruded from the cell by Na-K-ATPase located on the basolateral cell membrane. Chloride leaks into the lumen following a favorable electrical gradient. Potassium is thought to recirculate across the basolateral cell membrane. Since barium ions inhibit the efflux of potassium from cells we used barium chloride to explore the role of potassium in the process of stimulated secretion of chloride by the gland. The secretion of chloride was stimulated with theophylline 2.5 X 10(-4)M and dibutyryl cyclic AMP 5 X 10(-5)M. Ba++ inhibited the secretion of chloride in a way that was reversible and dose dependent. The reduction in secretion was associated with a parallel fall in transglandular electrical potential. Inhibition was half maximal at a concentration of Ba++ of 10(-3)M. The reduction in efflux of potassium produced by Ba++ presumably decreases the potassium diffusion potential, thus reducing the electronegativity of the cell and dissipating the driving force for chloride across the apical cell membrane. Recirculation of K+ across the basolateral border of the cell would thus be essential for the maintenance of chloride secretion by the gland.
 ...
PMID:Inhibition of chloride secretion by BaCl2 in the rectal gland of the spiny dogfish, Squalus acanthias. 394 77

Intracellular potential measurements of confluent monolayers of cultured bovine corneal endothelial cells were used to define passive ion transport processes in these cells. Previous studies (Jentsch et al., J. Membr. Biol. 78:103 (1984); Jentsch et al., J. Membr. Biol. 81:189 (1984] have provided the experimental basis for a cellular model, in which bicarbonate entry across the basolateral membrane is indirectly driven by a Na+/H+-exchanger, which is inhibitable by amiloride (1mM). Bicarbonate and sodium should leave the cell via an electrogenic bicarbonate sodium cotransport, which is inhibitable by the disulfonic stilbene derivates SITS or DIDS. This model is also consistent with results from transendothelial studies. In this paper, we briefly review the evidence we have obtained for this model and demonstrate, that the electrical response to sodium (depolarization upon Na+-removal) is neither due to an inhibition of Na+/K+-ATPase nor explainable in terms of changes in K+-conductance. This is concluded from the observation of these responses in the presence of ouabain (10(-4)M) or barium (1mM).
 ...
PMID:Ion transport mechanisms in cultured bovine corneal endothelial cells. 401 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>