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)

To evaluate the role of increased thick ascending limb Na+-K+-ATPase activity in rats undergoing hypertonic salt loading, the following groups of rats were studied: 1) control rats, 2) rats receiving an oral hypertonic Na load for 7 days, and 3) rats receiving the same oral Na load as in group 2 plus a daily injection of 10 mg/100 g of furosemide ip for 7 days. Salt loading (group 2) was associated with increased glomerular filtration rate (GFR) and hence an increased filtered load of sodium. Plasma aldosterone levels were markedly decreased. Na+-K+-ATPase was unchanged in the proximal tubule [convoluted (PC) and straight (PS)], increased in the thick ascending limb of Henle's loop [outer medullary (OMTAL) and cortical (CTAL)] and decreased in the distal nephron [distal convoluted tubule (DCT) and cortical collecting duct (CCD)]. The renal corticomedullary gradient of solutes was markedly increased in the salt-loaded group. Salt loading plus furosemide for 7 days (group 3) was associated with severe dehydration and hypernatremia. GFR as well as plasma aldosterone levels were unchanged compared with control. Na+-K+-ATPase was significantly increased in the proximal tubule (PC and PS), markedly decreased in the thick ascending limb of Henle's loop (OMTAL and CTAL), increased in the DCT and unchanged in the CCD. The increase in the corticomedullary gradient caused by salt loading per se was abolished by treatment of salt-loaded rats with furosemide. These results indicate that treatment with furosemide prevents the preservation of water balance and of normal body fluid tonicity in rats undergoing hypertonic Na loading.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Inhibition of thick ascending limb Na+-K+-ATPase activity in salt-loaded rats by furosemide. 253 44

In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.
...
PMID:Relationship between the sympathetic nervous system and sodium potassium adenosine triphosphatase inhibitor in salt-sensitive patients with essential hypertension. 285 28

Cardiopulmonary receptors influence renin release in a variety of physiological situations and in a fashion related to the degree of peripheral venous distensibility. We studied two groups of borderline hypertensives (BHTs) with different capacities to suppress plasma renin activity in response to saline infusion (0.20 mL/kg/per minute for 2 hours). Those BHTs with low suppressive capacity (L-supp) showed an increased venous distensibility in comparison with those with high suppressive capacity (H-supp). Saline infusion led to a significant increase in blood pressure only in L-supp BHTs, which was associated with enhanced 24-hour postloading natriuresis and raised plasma levels of an Na/K ATPase inhibitor (+12.2%). This result underlines the importance of venous distensibility as a determinant of pressor and humoral response to acute volume expansion.
...
PMID:Importance of plasma renin activity suppression and venous distensibility on pressor and natriuretic responses to intravenous salt load in borderline hypertension. 296 4

To compare the activity of Na-K-ATPase in the red blood cells (RBCs) and in renal tissue in disorders of Na+ metabolism, the following groups of rats were studied: 1) control, intact rats, 2) adrenalectomized (ADX) rats, 3) intact rats treated with DOCA, 4) ADX DOCA-treated rats, 5) intact salt-loaded rats, 6) ADX salt-loaded rats, 7) intact dexamethasone-treated rats (DEXA), and 8) ADX DEXA-treated rats. After adrenalectomy (group 2) serum Na+ decreased and serum K+ increased. Renal Na-K-ATPase in cortex, medulla and papilla of the control group was 44 +/- 2.7 mumol Pi/mg prot/h, 128.2 +/- 5.9 and 44 +/- 3.2 respectively and in group 2 the enzyme activity was 32.5 +/- 2.0 (P less than 0.005), 81.7 +/- 4.5 (P less than 0.001) and 23.6 +/- 1.9 (P less than 0.001) respectively. RBCs Na-K-ATPase of control animals was 2.82 +/- 0.19 mumol Pi/mg prot/h, while in group 2 the activity was 1.43 +/- 0.24 (P less than 0.001). DOCA treatment of ADX rats (group 4) normalized serum electrolytes and Na-K-ATPase activity in the renal cortex and papilla and in the RBCs. In the renal medulla the correction by DOCA was only partial. Salt loading of ADX rats (group 6) normalized serum electrolytes and Na-K-ATPase activity in the renal medulla and RBCs. Salt loading of normal rats increased RBC Na-K-ATPase to 3.72 +/- 0.36 (P less than 0.02) and medullary Na-K-ATPase to 185.6 +/- 9.8 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Parallel changes in red blood cell and renal Na-K-ATPase activity in adrenal and electrolyte disorders in the rat. 298 67

Cardiac glycosides bind to the Na+,K+-ATPase and inhibit its activity. Low concentrations (less than 10(-7) M) of ouabain stimulate the activity of Na+,K+-ATPase in whole homogenates of rat brain. The magnitude of this stimulation varies from 5 to 70%. The concentration of ouabain which induces maximal stimulation is also highly variable and ranges between 10(-9) to 10(-7) M. This stimulation may be explained by the presence of an endogenous ouabain-like compound (OLC) in the brain homogenate. Mammalian tissues and body fluids including brain, heart, kidney, plasma, urine and cerebrospinal fluid contain a unidentified OLC. An endogenous OLC was also demonstrated in toad skin and plasma. This compound was purified to homogeneity and identified using UV, NMR and Mass spectroscopies to be 3-hydroxy-14, 15-epoxy-20,22-dienolide glycoside (resibufogenin). Several reports have suggested that unsaturated fatty acids are the ouabain-like regulators of the Na+,K+-ATPase. Furthermore, Saline infusion to WKY rats, which was shown to increase OLC in the plasma causes also an elevation of free fatty acids. Thus, the interaction of fatty acids with several plasma membrane components was studied. Ouabain binding, opiate binding and binding to the beta-adrenergic receptor were all inhibited by micromolar concentrations of the unsaturated fatty acids, linoleic, oleic and arachidonic. Binding to the opiate receptor was inhibited with IC50 of 40-90 microM and binding to beta-adrenergic receptor with IC50 of 350-450 microM.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The ouabain receptor in animal tissues and its endogenous ligand. 303 84

Kinesin is a force-generating ATPase that drives the sliding movement of microtubules on glass coverslips and the movement of plastic beads along microtubules. Although kinesin is suspected to participate in microtubule-based organelle transport, the exact role it plays in this process is unclear. To address this question, we have developed a quantitative assay that allows us to determine the ability of soluble factors to promote organelle movement. Salt-washed organelles from squid axoplasm exhibited a nearly undetectable level of movement on purified microtubules. Their frequency of movement could be increased greater than 20-fold by the addition of a high speed axoplasmic supernatant. Immunoadsorption of kinesin from this supernatant decreased the frequency of organelle movement by more than 70%; organelle movements in both directions were markedly reduced. Surprisingly, antibody purified kinesin did not promote organelle movement either by itself or when it was added back to the kinesin-depleted supernatant. This result suggested that other soluble factors necessary for organelle movement were removed along with kinesin during immunoadsorption of the supernatant. A high level of organelle motor activity was recovered in a high salt eluate of the immunoadsorbent that contained only little kinesin. On the basis of these results we propose that organelle movement on microtubules involves other soluble axoplasmic factors in addition to kinesin.
...
PMID:The role of kinesin and other soluble factors in organelle movement along microtubules. 314 29

Certain factors that might contribute to the regulation of the rate of glycolysis by rat aorta were investigated. Rat aortic rings were incubated with [14C]glucose, and the release of [14C]lactate was determined. There was good agreement between the lactate production estimated by enzymatic assay and by [14C]lactate release, suggesting that almost all the lactate produced under our experimental conditions was derived from exogenous glucose. When the glucose concentration in the medium was 10 mM or higher, the rate of glucose transport did not limit the rate of lactate production. In most cases studies were done both aerobically and anaerobically. In Hanks' Balanced Salt Solution the aerobic rate of lactate production was 18% of the anaerobic rate. We tested the effects on glycolysis of agents that alter ATP generation by mitochondria or ATP splitting by Na+-K+-ATPase or the mitochondrial ATPase. Under aerobic conditions, ouabain (5 mM) caused a 54% decrease in lactate production, and gramicidin (5 micrograms/ml) caused a 45% increase. Under anaerobic conditions, neither ouabain nor gramicidin affected lactate production. Aerobically dinitrophenol (25 microM) and carboxyatractyloside (0.5 mM) caused substantial increases in lactate production, 72 and 98% respectively. Under anaerobic conditions the effects of dinitrophenol and carboxyatractyloside were much smaller, with dinitrophenol causing a 15% increase and carboxyatractyloside a 12% decrease in lactate production. Increasing the concentration of phosphate in the incubation medium caused marked increases in lactate production. Both aerobically and anaerobically, shifting from 1.3 to 50 mM phosphate in the incubation medium caused a 3.5-fold increase in lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Regulation of glycolysis in rat aorta. 620 40

Salt and water balance in vertebrates in controlled by the release of two blood borne hormones: aldosterone and antidiuretic (ADH). It is the purpose of this chapter to review the mechanisms (at the plasma membrane level) by which these hormones cause an increase in salt (sodium) and water movement in the target tissues. The primary effect of aldosterone is to increase the Na+ permeability of the lumen-facing (apical) membrane by activation of pre-existing quiescent channels at short times, and by the incorporation of newly synthesized channels after prolonged exposure. Other effects might involve an increase in energy supply and synthesis of Na+-K+ ATPase which is responsible for Na+ extrusion from cell cytoplasm to blood. Similarly, ADH stimulates pre-existing quiescent apical membrane Na+ channels. The second effect of ADH is to increase epithelial water permeability. Evidence strongly suggests that water channels exist in cytoplasmic vesicles which, upon ADH challenge, fuse into the apical membrane causing a rapid increase in apical membrane hydraulic conductivity. The movements of vesicles are dependent on an intact cytoskeleton. Regulation of electrolyte and non-electrolyte transport will be discussed in the light of the above two mechanisms.
...
PMID:Control of Na+ and water absorption across vertebrate "tight epithelia by adh and aldosterone. 631 91

Sodium chloride transfer across isolated frog skin is described by the well-known Koefoed Johnsen-Ussing (KU) model, the central features of which are 1) a two-step, active, inward transport of Na+, and 2) passive cotransfer of Cl-, which is coupled electrically to Na+ movement under open-circuit conditions. However, NaCl absorption by the frog skin in vivo involves active inward transport of both ions by completely independent systems. Electrical neutrality is maintained by countertransfer of H+ (exchanged for Na+) and HCO-3 (exchanged for Cl-). This behavior is called the Krogh (KR) model. The KU and KR models share some features, notably amiloride sensitivity and participation of the Na+-K+-ATPase in Na+ transport, but the differences between them are fundamental. The latter appear to be due to the use of different experimental conditions. Intact frogs are usually studied in dilute (approximatley 1 mM) external solutions, while Ringer solution is used in most work on isolated skins. The skin is virtually impermeable to Cl- in dilute external media but permeable in Ringer solution. This concentration-dependent change in PCl can explain most of the differences between KU and KR models. Regulation of blood NaCl concentration in freshwater aquatic animals requires active uptake of both Na+ and Cl-. Data on representatives of four phyla show that the KR model describes the transport behavior in all of them. Such similarities in unrelated animals suggest that the transport mechanisms evolved very early in marine ancestors of modern freshwater forms. The implications of this suggestion are considered.
...
PMID:Sodium chloride absorption across the body surface: frog skins and other epithelia. 634 May 29

Salt transport by the Necturus gallbladder epithelium is the result of the coupled entry of NaCl into the cells across the apical membrane and the active transport of Na out of the cells across the basolateral membrane. The NaCl entry step was studied by measuring the rate of cell volume increase accompanying ouabain inhibition of the Na--K-ATPase in the basolateral membrane. When bumetanide, a diuretic analog of furosemide, was added to the mucosal bathing solution it reversibly blocked the entry of NaCl into the cells and abolished fluid transport. A dose-response relationship showed half-maximal inhibition of NaCl entry at a bumetanide concentration of 10(-9) M; complete inhibition of coupled NaCl movement occurred with as little as 10(-7) M bumetanide. Partial substitution of Na or Cl in the mucosal solution failed to demonstrate competition between bumetanide and either of the ions. The drug was also effective in blocking NaCl entry in the absence of ouabain; addition of the diuretic to the mucosal bathing solution resulted in prompt cell shrinkage and a decrease in intracellular NaCl. Cell volume decrease followed bumetanide addition to the mucosal bath because NaCl entry was blocked but active Na transport continued for several minutes until the intracellular Na transport pool was depleted.
...
PMID:Bumetanide inhibition of NaCl transport by Necturus gallbladder. 687 47


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

---