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At least 973 records · Page 54Linked to original sources
PubMed1991

Effects of chronic manganese treatment on rat brain regional sodium-potassium-activated and magnesium-activated adenosine triphosphatase activities during development.

The effects of chronic manganese (Mn) treatments (1 and 10 mg MnCl2.4H2O per ml of drinking water) from conception onwards on brain regional development of sodium-potassium-activated and magnesium-activated adenosine triphosphatases (Na-K-ATPase and Mg-ATPase) were studied. The activities of these enzymes were determined in hypothalamus, cerebellum, pons and medulla, striatum, midbrain and cerebral cortex (which included the hippocampus) of Mn-treated and age-matched control rats at 5 postnatal ages. Both ATPase activities doubled in most brain regions between day 5 and day 20 postnatal. In pons and medulla, striatum, midbrain, and cerebral cortex, adult levels of both enzymatic activities were attained by day 20 postnatal. Na-K-ATPase activities transiently increased in the midbrain (+25%) at day 12 with the lower Mn dose and in the cerebral cortex (+31%) at day 20 with the higher Mn dose. With the higher Mn dose only, Mg-ATPase activities were increased in the hypothalamus (+20%) at day 12 and in the pons and medulla (+22%) at day 20 but were decreased in the pons and medulla (-20%) at day 60. Thus, only transient changes in enzymatic activities were observed despite dose-dependent increases in the brain levels of Mn resulting from the Mn treatment. A hypothesis regarding the role of early but transient changes in brain metabolism in the pathogenesis of the initial psychotic symptoms in Mn intoxication was proposed and discussed in relation to several other observations of a similar nature.

Age Factors↗
PubMed1999

Gastric H(+),K(+)-adenosine triphosphatase beta subunit is required for normal function, development, and membrane structure of mouse parietal cells.

BACKGROUND & AIMS: Parietal cells of the gastric mucosa contain a complex and extensive secretory membrane system that harbors gastric H(+),K(+)-adenosine triphosphatase (ATPase), the enzyme primarily responsible for acidification of the gastric lumen. We have produced mice deficient in the H(+),K(+)-ATPase beta subunit to determine the role of the protein in the biosynthesis of this membrane system and the biology of gastric mucosa. METHODS: Mice deficient in the H(+), K(+)-ATPase beta subunit were produced by gene targeting. RESULTS: The stomachs of H(+),K(+)-ATPase beta subunit-deficient mice were achlorhydric. Histological and immunocytochemical analyses with antibodies to the H(+),K(+)-ATPase alpha subunit revealed that parietal cell development during ontogeny was retarded in H(+), K(+)-ATPase beta subunit-deficient mice. In 15-day-old mice, cells with secretory canaliculi were observed in wild-type but not in H(+), K(+)-ATPase beta subunit-deficient mice. Parietal cells of H(+), K(+)-ATPase beta subunit-deficient mice 17 days and older contained an abnormal canaliculus that was dilated and contained fewer and shorter microvilli than normal. In older parietal cells, the abnormal canaliculus was massive (25 micrometer in diameter) and contained few microvilli. We did not observe typical tubulovesicular membranes in any parietal cell from H(+),K(+)-ATPase beta subunit-deficient mice. Histopathologic alterations were only observed in the stomach. CONCLUSIONS: The H(+),K(+)-ATPase beta subunit is required for acid-secretory activity of parietal cells in vivo, normal development and cellular homeostasis of the gastric mucosa, and attainment of the normal structure of the secretory membranes.

Animals↗
PubMed1985

Na+,K+-activated adenosine triphosphatase of isolated Müller cells from the rabbit retina shows a K+ dependence similar to that of brain astrocytes.

Müller (glial) cells from the rabbit retina were isolated by means of papain and mechanical dissociation. Their Na+,K+-adenosine triphosphatase (ATPase) activity was measured using a radiochemical method, and its K+ dependence was determined. In contrast to that of photoreceptors (data from the literature), the Na+,K+-ATPase of Müller cells could be shown to increase its activity greatly when the [K+] was enhanced up to 10 mM. The functional implications of this behaviour for the K+ clearance in the retina are discussed.

Animals↗
PubMed1997

Evidence for the presence of sodium- and potassium-dependent adenosine triphosphatase alpha1 and beta1 subunit isoforms and their probable role in blastocyst expansion in the preattachment horse conceptus.

The unusual hypotonicity of equine blastocyst fluid has prompted us to investigate the role of sodium- and potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) in the process of fluid accumulation in the horse conceptus. Nine mares were used for the experiments. Reverse transcriptase polymerase chain reaction was conducted on two sets of five conceptuses recovered between 12 and 28 days (+/- 1 day) after ovulation. Messenger RNAs encoding the alpha1 and beta1 subunit isoforms of Na+,K+-ATPase were detected in all embryonic tissues examined. Western blot analysis showed that alpha1 and beta1 subunits are both present in Day 15 conceptuses. Trophoblast tissues from 19 conceptuses between 8 and 31 days after ovulation were stained immunohistochemically using primary antibodies against the alpha1 and beta1 subunit isoforms of the Na+,K+-ATPase. Both isoforms were detected in all sections. Trophoblastic vesicles, prepared from 6 conceptuses between 12 and 14 days after ovulation, were used to investigate the inhibition of blastocyst expansion with ouabain after collapse induced with cytochalasin D. In normal medium there was a mean 3-fold increase, and in ouabain (10(-6) M) a mean 3-fold decrease, in the volume of vesicles that had been partially collapsed with cytochalasin D. We therefore conclude that, despite the hypotonicity of the blastocyst fluid in the early horse conceptus, the Na+,K+-ATPase plays a role in its accumulation, as in other species.

Animals↗
PubMed1991

Expression and distribution of renal vacuolar proton-translocating adenosine triphosphatase in response to chronic acid and alkali loads in the rat.

Renal hydrogen ion excretion increases with chronic acid loads and decreases with alkali loads. We examined the mechanism of adaptation by analyzing vacuolar proton-translocating adenosine triphosphatase (H+ ATPase) 31-kD subunit protein and mRNA levels, and immunocytochemical distribution in kidneys from rats subjected to acid or alkali loads for 1, 3, 5, 7, and 14 d. Acid- and alkali-loaded rats exhibited adaptive responses in acid excretion, but showed no significant changes in H+ ATPase protein or mRNA levels in either cortex or medulla. In contrast, there were profound adaptive changes in the immunocytochemical distribution of H+ ATPase in collecting duct intercalated cells. In the medulla, H+ ATPase staining in acid-loaded rats shifted from cytoplasmic vesicles to plasma membrane, whereas in alkali-loaded rats, cytoplasmic vesicle staining was enhanced, and staining of plasma membrane disappeared. In the cortical collecting tubule, acid loading increased the number of intercalated cells showing enhanced apical H+ ATPase staining and decreased the number of cells with basolateral or poorly polarized apical staining. The results indicate that both medulla and cortex participate in the adaptive response to acid and alkali loading by changing the steady-state distribution of H+ ATPase, employing mechanisms that do not necessitate postulating interconversion of intercalated cells with opposing polarities.

Acid-Base Equilibrium↗
PubMed1970

Adenosine Triphosphatase Activities in Leaves of the Mangrove Avicennia nitida Jacq: Influence of Sodium to Potassium Ratios and Salt Concentrations.

Homogenates from the salt-excreting leaves of the mangrove Avicennia nitida were subjected to differential centrifugation and investigated for adenosine triphosphatase activities. At pH 6.75 a salt stimulation with peaks at three different sodium to potassium ratios could be demonstrated above the activity due to Mg(2+) ions. The stimulation by sodium and potassium depends on the ionic strength of the test medium, higher salt concentrations being inhibitory. The plant system seems thus more complicated than the animal activities. Technically, this means that a search for (Na(+) + K(+))-activated ATPases in plants should be performed with a close spacing of Na:K ratios at several constant levels of salt. Literature data on the transport of Na(+) and K(+) indicate that the physiological situation is rather complex in plants.

Journal Article↗
PubMed1992

The identification, purification, and characterization of a pancreatic beta-cell form of the microtubule adenosine triphosphatase kinesin.

Microtubules have been implicated as being necessary for the secretion of insulin from beta-cells, although the mechanism by which cytoplasmic microtubules contribute to the release of insulin is unknown. Kinesin is a microtubule-dependent adenosine triphosphatase (ATPase) that is thought to be responsible for the intracellular transport of vesicles and organelles. In this manuscript, the purification and preliminary characterization of a beta-cell form of kinesin is described. A 120-kilodalton antikinesin-reactive polypeptide was identified on blots when cultured insulinoma tumor cell lines were subjected to immunoblot analysis using monoclonal antibodies specific for the heavy chain of mammalian kinesin. The beta-cell form of kinesin was isolated from solid rat insulinoma tumors by cosedimentation of the kinesin with microtubules from tissue homogenates in the presence of adenylyl-imidodiphosphate. The beta-cell kinesin was further purified by gel filtration chromatography, and then the pure enzyme was characterized using in vitro assays. Although beta-cell kinesin showed little ATPase activity alone, the enzyme exhibited considerable ATP hydrolysis activity in the presence of taxol-stabilized microtubules. Moreover, in motility assays beta-cell kinesin was able to translocate microtubules across microscope coverslips in the presence of Mg(2+)-ATP. In summary, we report the identity of a novel islet beta-cell form of the microtubule-dependent ATPase kinesin and suggest a possible contribution of the microtubule cytoskeleton in insulin secretion.

Animals↗
PubMed1979

Calcium ion-dependent adenosine triphosphatase activity and plasma-membrane phosphorylation in the human neutrophil.

A plasma-membrane fraction was isolated from a post-nuclear extract of human neutrophils by centrifugation through a linear sucrose density gradient. This fraction exhibited a Ca2+-dependent adenosine triphosphatase (ATPase) activity that could be differentiated from mitochondrial or myosin ATPase and from plasma-membrane Mg2+-dependent ATPase. When assayed in the presence of [gamma-32P]ATP, the Ca2+-dependent ATPase reaction resulted in the formation of an acid-resistant hydroxylamine-sensitive bond between the gamma-[32P] phosphate group and a membrane protein subunit with an apparent mol.wt. of 135000. Half-maximal activating effect of Ca2+ was found at 82nM and 0.18 microM for the ATPase and the formation of the 32P-membrane complex respectively. Generation of the phosphorylated product attained the steady state at 0 degrees C by about 30s, and was rapidly reversed by ADP. These results suggest that the Ca2+-activated ATPase reaction occurs through the formation of a phosphoprotein intermediate, similar to that described for some Ca2+-dependent ATPase enzymes associated with Ca2+ transport. The possibility thus exists that the neutrophil Ca2+-dependent ATPase catalyses a process of Ca2+ extrusion from the cell, thereby participating in the regulation of several Ca2+-dependent neutrophil functions.

Adenosine Triphosphate↗
PubMed1980

Erythrocyte ghost Na+,K+-adenosine triphosphatase in Duchenne muscular dystrophy.

Erythrocyte ghost membranes have been prepared by two different methods from patients with Duchenne muscular dystrophy (DMD), carriers of DMD, patients with other neuromuscular diseases, and normal individuals. The susceptibility of the membrane Na+,K+-adenosine triphosphatase (ATPase) to the cardiac glycoside, ouabain, has been investigated using various assay conditions. A stimulation of the enzyme has not been detected under any of the conditions employed. Using either a "high salt" (100 mM NaCl, 20 mM KCl) or a "low salt" (1 mM NaCl, 2 mM KCl) assay in the presence of EGTA a reduced susceptibility of the enzyme to ouabain was observed in preparations from patients with DMD compared with those from normal individuals. This behaviour was not manifest in preparations from NAD carriers or from patients with other neuromuscular diseases. The response of the erythrocyte membrane Na+,K+-ATPase activity to changes in temperature has also been investigated. The temperature response of the enzyme from DMD and DMD carrier preparations was indistinguishable from that of normal preparations. In all cases a break in the Arrhenius plot occurred at 21 degrees C.

Adolescent↗
PubMed1998

Alpha 2 isoform of the Na,K-adenosine triphosphatase is reduced in temporal cortex of bipolar individuals.

BACKGROUND: The pathophysiology of bipolar illness has been associated with changes in transmembrane ion flux and redistribution of biologically active ions. The recent identification of multiple isoforms of Na,K-adenosine triphosphatase (ATPase) alpha and beta subunits raises the possibility of altered pump isoform expression. METHODS: We determined Na,K-ATPase alpha subunit expression in postmortem temporal cortex gray matter from individuals suffering from bipolar disorder, schizoaffective disorder, schizophrenia, and matched normal controls. Quantification of isoform expression was accomplished via densitometric scanning of Western blots utilizing isoform-specific antibodies. RESULTS: Bipolar individuals exhibited a significant reduction in the abundance of the alpha 2 isoform of Na,K-ATPase compared to normal controls. Schizophrenic and schizo-affective brains were not significantly different from normal controls. CONCLUSION: These data suggest that previously observed abnormalities in regulation and distribution of ions in bipolar illness may be related to specific alpha 2 dysregulation.

Bipolar Disorder↗
PubMed1980

The primary structure of the calcium ion-transporting adenosine triphosphatase protein of rabbit skeletal sarcoplasmic reticulum. Peptides derived from digestion with cyanogen bromide, and the sequences of three long extramembranous segments.

The isolation and characterization of the soluble peptides from the CNBr digest of the calcium ion-transporting adenosine triphosphatase protein of rabbit skeletal sarcoplasmic reticulum are described. The 562 unique residues of the protein were placed in sequences. The remaining part of the protein (about 500 residues) yielded long hydrophobic sequences that contained all but one of the tryptophan residues of the protein and that were probably derived largely from the intramembranous parts of the protein. Three long stretches of primary structure, constituting half of the protein, have been reconstructed from the information presented here together with the sequences found in peptides from other digests of the protein. The secondary structures of these sequences have been predicted. A model for the primary structure of the protein is presented and the implications discussed. Details of the isolation of peptides are contained in Supplementary Publication, SUP 50105 (29 pages), which has been deposited with the British Library Lending Division, Boston Spa, Wetherby, West Yorkshire LS23 7BQ, U.K., from whom copies can be obtained on the terms indicated in Biochem. J. (1978) 169, 5.

Amino Acid Sequence↗
PubMed1987

Intracisternal administration of pergolide, a dopamine receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase and enhances vascular reactivity in anaesthetized dogs.

1. The present studies were undertaken to investigate whether intracisternal administration of pergolide, a dopamine-2 receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase into the circulation and whether such an effect is associated with increases in vascular reactivity in pentobarbital anaesthetized dogs. In different groups of animals, Na+-pump activity was estimated in the plantar and dorsal branches of the lateral saphenous veins by using the 86Rb-uptake method; vascular responsiveness to noradrenaline was studied in the denervated perfused hindlimb. 2. Na+-pump activity was significantly depressed in those blood vessels which were collected at 90 min after central administration of pergolide (12.5 micrograms/kg intracisternally). In perfused hindlimb studies, vascular responses to noradrenaline were significantly enhanced between 60 and 90 min after pergolide. Since the Na+-pump activity was evaluated in the hindlimb veins, and vascular reactivity was studied on the arterial circulation, the data suggest that the changes in both these variables could have been caused by a circulating substance. 3. In separate series of experiments, plasma samples were collected before and after intracisternal administration of pergolide. The Na+-pump activity was significantly inhibited in the segments of lateral saphenous veins which were incubated in the fresh plasma and/or boiled plasma supernatants, indicating that a heat stable pump inhibitor(s) is released into the circulation after pergolide administration. 4. Effects of pergolide demonstrated in the present study are qualitatively similar to those reported to occur after acute blood volume expansion. Hence it is proposed that central dopaminergic mechanisms may play an intermediary role in the release of the Na+-pump inhibitor(s).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Studies on the role of sodium- and potassium-activated adenosine triphosphatase inhibition in the pathogenesis of human hypertension. Changes in vascular and cardiac function following inhibition of the sodium pump in normotensive subjects and effects of calcium entry blockade.

An endogenous humoral factor which inhibits the sodium- and potassium-activated adenosine triphosphatase (Na-K-ATPase) enzyme in vitro has been incriminated recently of playing a pathogenetic role in experimental and human hypertension. The present study was therefore performed in six healthy volunteers to investigate the hemodynamic consequences of an inhibition of this enzyme by ouabain, a potent and specific inhibitor of Na-K-ATPase. In addition, the role of intracellular calcium as a potential mediator was studied indirectly by the administration of nifedipine, a potent calcium entry blocker with predominant vasodilator properties. Intravenous administration of 8.5 micrograms ouabain/kg body weight inhibited red blood cell (RBC) - Na-K-ATPase by 49% which was accompanied by a significant increase in RBC - ATP and a decrease in intracellular potassium concentrations. This enzyme inhibition resulted in a 24% increase in peripheral vascular resistance. The parallel decrease in cardiac output and heart rate, however, prevented a rise in arterial pressure. This increase in vascular resistance was completely abolished by pretreatment with nifedipine (10 mg orally). In the absence of an effect of nifedipine on Na-K-ATPase, its attenuation of the vasoconstrictor effect of ouabain suggests that the effects of ouabain on the vascular smooth muscle cell are mediated by intracellular calcium. These results demonstrate that inhibition of the Na-K-ATPase enzyme in vivo causes a marked peripheral vasoconstriction. They are also compatible with the concept that an endogenous inhibitor of Na-K-ATPase - in the presence of decreased baroreceptor reflex sensitivity due to blood volume expansion - may play a role in the pathogenesis of human arterial hypertension.

Adenosine Triphosphate↗
PubMed1999

H+/K+-adenosine triphosphatase mRNA in gastric fundic gland mucosa in patients infected with Helicobacter pylori.

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion has not been made clear. This study aimed to elucidate the effects of H. pylori infection on H+/K+-adenosine triphosphatase (ATPase) mRNA in gastric fundic gland mucosa. METHODS: Twenty patients with chronic gastritis and H. pylori infection were treated with lansoprazole and antibiotics. Before and 1 month after treatment gastroduodenoscopy was performed, and changes in the amount of H+/K+-ATPase mRNA in the fundic gland mucosa, gastric juice pH, and serum gastrin levels were determined. RESULTS: The amount of H+/ K+-ATPase mRNA in the fundic gland mucosa was increased in patients with eradication of H. pylori, in whom significant decreases in gastric juice pH and serum gastrin levels were observed. No significant changes were observed in patients without eradication of H. pylori. CONCLUSIONS: These results suggest that one of the mechanisms by which H. pylori infection suppresses acid secretion is by the inhibition of proton pump synthesis in parietal cells.

DNA Primers↗