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

---

Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mineralocorticoid steroids markedly alter ion transport in responsive epithelia. Increases in absorption of Na+ and secretion of K+ and H+ are accompanied by increases in surface area of the basolateral membrane. The basolateral membrane changes are associated with increased Na(+)-K(+)-ATPase activity and increased numbers of Na(+)-K(+)-ATPase pump sites. It is thought that H+ secretion is mediated by H+ pumps contained in apical vesicles that are added to the luminal membrane in response to acidifying stimuli. Whether there are changes in the number or volume of apical vesicles in response to aldosterone has not been evaluated. To this purpose, we evaluated apical membrane morphology in rat distal colon, a mineralocorticoid-responsive epithelium. We found that aldosterone infused for 4-7 days by osmotic minipump significantly increased the number, surface density, and total volume of apical vesicles. Exposure of tissues to 5% CO2 for 15 min before fixation resulted in significant decreases in vesicle number, surface density, and volume in aldosterone-stimulated tissues. After CO2, apical vesicles in aldosterone-stimulated tissues tended to be closer to the luminal membrane; apical membrane surface density was increased but not to a significant degree. Fluorescence microscopy demonstrated acridine orange accumulation in discrete points under the lumen, suggesting the presence of acidic vesicles in this location. We propose that aldosterone increases the activity of a membrane shuttle system that is regulated by CO2 as found in other H(+)-secreting epithelia. This system may mediate aldosterone-induced changes in colonic H+ transport.
...
PMID:Aldosterone induces apical vesicles in rat distal colon. 211 40

Carbonic anhydrase (CA) and Mg2(+)-dependent ATPase and Mg2(+)-dependent, HCO3(-)-stimulated ATPase (Mg2(+)-HCO3(-)-ATPase) activities in rat duodenal mucosa and kidney cortex were examined with respect to thyroidal status. Administration of 50 and 150 micrograms thyroxine (T4)/kg per day s.c. for 7 days decreased duodenal cytosol CA activity to 66% of control with the former and 43% with the latter dose, while Mg2(+)-HCO3(-)-ATPase activity in brush borders of duodenal mucosa was increased to 116% of control by 150 micrograms T4/kg. CA and Mg2(+)-HCO3(-)-ATPase activities in the cytosol and brush border of kidney cortex did not change after administration of T4. Hypothyroidism induced by thyroidectomy for 2 and 4 weeks or administration of methimazole (2.5-20 mg/kg per day s.c. or peroral) for 2, 3 and 4 weeks all increased duodenal cytosol CA activity, to about 140% at 2 weeks and 153% at 4 weeks after thyroidectomy, and to about 136% after the oral administration of 10 mg methimazole/kg per day for 4 weeks, while brush border Mg2(+)-HCO3(-)-ATPase activity was decreased to 56% of control 4 weeks after thyroidectomy and to 74% after the s.c. administration of 20 mg methimazole/kg day for 3 weeks. The increase in CA activity and the decrease in ATPase activity after thyroidectomy were restored to normal levels by replacement with T4. Neither enzyme activity in the kidney changed in hypothyroidism. Serum concentrations of T4 and cortisol-like material increased after administration of T4, and serum concentrations of T4, aldosterone and cortisol-like material all decreased in hypothyroidism. Correlations were observed between duodenal CA and Mg2(+)-HCO3(-)-ATPase activities and serum concentrations of T4 (P less than 0.01). These results reveal that the decrease in CA activity and the increase in Mg2(+)-HCO3(-)-ATPase activity of duodenal mucosa in hyperthyroidism are reversed in hypothyroidism, while both enzyme activities in the kidney are unrelated to thyroidal status.
...
PMID:Effects of hyper- and hypothyroidism on carbonic anhydrase, Mg2(+)-dependent ATPase and Mg2(+)-dependent, HCO3(-)-stimulated ATPase activities of rat duodenal mucosa and kidney cortex. 214 14

Aldosterone increased the tubular volume in cortical collecting tubules (CCD) of rabbit kidney. It modulated the rate of cell sodium accumulation, under condition of ATPase inhibition (4 degrees C, in the absence of K+). In contrast, the relationship between Na+/K(+)-ATPase-dependent Na+ extrusion rate and intracellular Na+ concentration (Nai+) was similar in control, adrenalectomized, and aldosterone-treated adrenalectomized animals: Na+ extrusion rate increased with Nai+, up to 70 mM Nai+, and then plateaued. This indicates that aldosterone does not modify the characteristics of Nai(+)-dependent Na+ extrusion rate by the Na+/K(+)-ATPase pump in CCD.
...
PMID:Effect of cell sodium on Na+/K(+)-ATPase-dependent sodium efflux in cortical collecting tubule of rabbits under different aldosterone status. 215 60

The present study was conducted in 15 essential hypertensives to evaluate the modifications of plasma levels of an endogenous Na/K ATPase inhibitor, blood pressure, forearm hemodynamics and plasma renin activity (PRA) elicited by an intravenous saline infusion (0.9% NaCl at the mean rate of 0.22 mL/min/kg body weight for 2 h). The response to saline was determined in the whole hypertensive population as well as in two subgroups of patients classified according to their rate of PRA suppression in response to volume expansion by comparison with normotensive controls (Normal- and Low-suppressors: N-S, L-S). Over the whole group of hypertensive patients, NaCl load provoked an increase in Na/K ATPase inhibitory activity, measured by enzyme-coupled assay, which was linearly related to PRA decline (r = 0.73) and to the increase in mean blood pressure (r = 0.57). These effects were clearly enhanced by considering L-S patients alone. Urinary Na/K ratio after saline infusion was significantly higher in L-S as result of a lesser potassium excretion in this subgroup. Our results support the hypothesis that acute volume expansion with saline causes an increase in plasma levels of an endogenous sodium pump inhibitor with hemodynamic effects and whose release is related to the individual handling of infused fluids and to the degree of renin-angiotensin-aldosterone suppression.
...
PMID:Short-term plasma renin activity suppression by saline and release of a plasma endogenous Na/K ATPase inhibitor in essential hypertension. 215 4

Mineralocorticoids and glucocorticoids exhibit overlapping but distinct effects on transepithelial sodium transport in the descending colon. Na,K-ATPase, the major sodium pump, has been variously reported to be regulated by one or both classes of steroids. The present studies explore the ontogeny and steroidal regulation of Na,K-ATPase alpha- and beta-subunit mRNA levels in the descending colon. In descending colon, subunit mRNA levels are low before birth, increasing to reach adult levels at approximately day 25. Dexamethasone treatment caused a rapid dose-dependent increase in colonic Na,K-ATPase subunit mRNA levels. The specific glucocorticoid RU26988 also increased subunit mRNA levels. Aldosterone administration, at doses adequate to yield a profound antinatriuresis, did not alter subunit mRNA levels. Carbenoloxone sodium produced an approximately 3-fold increase in subunit mRNA levels in intact but not adrenalectomized rats. We have demonstrated that Na,K-ATPase subunit gene expression is: 1) low in the fetal colon but achieves plateau levels by day 25; 2) acutely regulated by corticosteroids via type II rather than type I receptors; and 3) increased by carbenoxolone sodium, presumably as a result of increased occupancy of the type II receptor by corticosterone.
...
PMID:Colonic sodium-potassium adenosine triphosphate subunit gene expression: ontogeny and regulation by adrenocortical steroids. 216 14

The influence of intracellular sodium concentration ( [Na+]i) on the number of Na(+)-K(+)-ATPase pumps was examined in cortical collecting tubules (CCD) of kidneys from rabbits in different aldosterone conditions. Specific [3H]ouabain binding was measured in isolated CCD with various [Na+]i. Experiments were performed on adrenalectomized rabbits receiving only a substitutive dose of dexamethasone and on adrenalectomized rabbits replete with aldosterone. In aldosterone-replete rabbits, the number of binding sites increased linearly with [Na+]i, from 16 fmol/nl tubular volume at 15 mM Na+i to 39 fmol/nl tubular volume at 140 mM Na+i. Neither actinomycin D (5 microM) nor cycloheximide (10 microM) prevented this [Na+]i-dependent increase. In adrenalectomized rabbits, the number of ouabain-binding sites was reduced and did not increase with [Na+]i. These results are in favor of the presence of a "latent" pool of pumps in CCD, rapidly recruited under [Na+]i influence. Aldosterone appears to be required for the constitution and/or activation of this pool.
...
PMID:Cell sodium-induced recruitment of Na(+)-K(+)-ATPase pumps in rabbit cortical collecting tubules is aldosterone-dependent. 216 11

Sustained exposure to aldosterone (Aldo) increases the abundance and activity of the Na-K pump in cortical collecting tubules (CCT). However, the onset and mechanism of the early interaction of Aldo with the CCT pump, especially in adrenal-intact animals, are unclear. We evaluated the short-term effects of the hormone on Na-K-adenosinetriphosphatase (ATPase) activity and on ouabain-sensitive 86Rb uptake, a measure of the transporting rate of the pump, in microdissected CCT from adrenal-intact rats. Incubation with Aldo (10(-8) M, 2 h) had no effect on Na-K-ATPase activity (Vmax), whereas it produced at least a twofold increase in 86Rb uptake. This effect was generated by physiological concentrations of the hormone (threshold 10(-10) M; apparent K1/2 approximately 10(-9) M), after a short lag of less than or equal to 30 min. Incubation with Aldo in the presence of amiloride or nystatin or in a Na-free medium (choline chloride) did not prevent the enhanced 86Rb uptake seen after Aldo alone; possible interpretations of these observations are discussed. We conclude that Aldo produces a rapid stimulation of pump function in CCT that precedes its induction of new pump synthesis; the physiological significance of this effect is suggested by its occurrence in tubules from adrenal-intact animals within the time frame and concentration range of the hormone's effects on electrolyte transport.
...
PMID:Early effects of aldosterone on Na-K pump in rat cortical collecting tubules. 216 59

The aldosterone-induced up-regulation of Na absorption and K secretion in the CCD is complex and involves the regulation of numerous transport proteins. Some aspects of the response may be species dependent. For example, stimulation of Na and K transport in the rabbit CCD involves a marked up-regulation in the apical cell membrane Na and K conductances, the basolateral cell membrane K conductance, and the basolateral membrane NaK-ATPase activity. In the rat CCD, aldosterone causes a similar up-regulation in the NaK-ATPase and the apical membrane Na conductance, but supposedly has little influence on the apical and basolateral membrane K conductances as evaluated by indirect methods. Furthermore, the marked hyperpolarization of the basolateral membrane with long-term aldosterone treatment in the rabbit CCD is blunted or absent in the rat CCD. Other differences between the CCD of these two species have been outlined. Nonetheless, the basic responses of the CCDs from the two species show similar trends. The actions of aldosterone in the CCD principal cell are summarized in Figure 5. The initial steps have been described previously. Aldosterone (A) diffuse across the cell membrane and binds to a cytoplasmic receptor (R). The receptor complex moves into the nucleus and binds to an acceptor site on chromatin, initiating transcription and the subsequent synthesis of a myriad of new proteins referred to as aldosterone-induced proteins (AIP). The initial observed action of aldosterone is an upregulation of the apical membrane Na conductance during the early phase, which occurs within 1 to 2 hours. The increase in Na conductance likely reflects activation of preexisting latent Na channels and not synthesis of new channels, although activation does require protein synthesis. The increased Na influx during the early phase presents a larger Na load to the Na pump, which is likely reflected as a modest transient increase in intracellular Na activity. Based on kinetic considerations alone, this should cause an increased transport turnover of the pump with a greater Na extrusion rate and K uptake rate. The stimulated Na influx also causes a modest depolarization of the apical membrane during the early phase, which when combined with the increased K uptake via the pump and an apparent modest elevation in the intracellular K activity, results in a more favorable gradient for K secretion (increased driving force) into the tubule lumen.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Aldosterone regulation of sodium and potassium transport in the cortical collecting duct. 216 26

The Madin-Darby canine kidney (MDCK) cell line was used to evaluate the influence of high extracellular K+, independent of hormonal effects, on renal Na-K-adenosinetriphosphatase (ATPase) activity and abundance. Confluent cell monolayers were incubated in control (5 mM) or high K+ (7.5 mM) medium for 24 h. Exposure to high K+ elicited a 46% rise in Na-K-ATPase activity and a 55% increase in ouabain-sensitive 86Rb uptake. Na-K-ATPase abundance, estimated from the number of ouabain-binding sites, also increased 63% over control in cells exposed to 7.5 mM K+, and as a consequence there was no statistically significant change in the catalytic turnover number. Northern blot analysis using rat cDNA probes for the alpha 1- and beta-subunits showed no corresponding changes in subunit-specific mRNA abundances at 24 h. We conclude that chronic exposure to high extracellular K+ produces a rise in renal epithelial Na-K-ATPase activity and active K+ transport, independent of changes in aldosterone, renal blood flow, or extracellular Na+ concentration. This effect is due to an increase in enzyme abundance rather than a change in catalytic turnover rate. The results of Northern analysis suggest that regulation of Na-K-ATPase activity and abundance by high K+ may involve translational or posttranslational mechanisms, but further study with cDNA probes of canine origin is needed to resolve this issue.
...
PMID:Effect of high extracellular K+ on Na-K-ATPase in cultured canine kidney cells. 216 14

The ability of urine extracts to inhibit sodium and potassium-activated ATPase, cross-react with antidigoxin antibodies and induce natriuresis in rats was investigated in 10 healthy subjects, 10 cirrhotic patients without ascites (compensated cirrhotics), 27 nonazotemic cirrhotic patients with ascites and 10 cirrhotic patients with ascites and functional renal failure to assess whether reduced activity of natriuretic hormone contributes to sodium retention in cirrhosis. No significant differences were seen between healthy subjects and compensated cirrhotic patients in any of these parameters (sodium and potassium-activated ATPase inhibition = 178.5 +/- 19.8 vs. 247.4 +/- 48.7 nmol equivalent of ouabain/day; digoxinlike activity = 43.9 +/- 6.1 vs. 48.0 +/- 5.6 ng equivalent of digoxin/day; natriuretic activity = 0.36 +/- 0.15 vs. 0.63 +/- 0.27 mumol/min). Cirrhotic patients with ascites with and without functional renal failure showed significantly higher values of sodium and potassium-activated ATPase inhibition (708.1 +/- 94.0 and 529.2 +/- 53.9 nmol equivalent of ouabain/day, respectively), digoxinlike activity (136.9 +/- 7.2 and 116.3 +/- 7.9 ng equivalent of digoxin/day) and natriuretic activity (1.78 +/- 0.48 and 1.93 +/- 0.37 mumol/min) than healthy subjects and compensated cirrhotic patients. We saw no significant differences between these two groups of cirrhotic patients with ascites with respect to these parameters. In the cirrhotic patients studied, sodium and potassium-activated ATPase inhibition and antidigoxin antibodies directly correlated with the degree of impairment of hepatic and renal function, plasma renin activity and plasma levels of aldosterone and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Natriuretic hormone activity in the urine of cirrhotic patients. 216 51


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

---