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)

In vasogenic cerebral oedema, there is progressive quantitative and qualitative impairment of mitochondrial ATPase and of Na/K/ATPase. This impairment, which reflects the intracellular component of cerebral oedema, would appear to be related to changes in the phospholipid environment of the cell membrane enzymes. CDP choline, a metabolic phospholipid precursor, is to a certain extent capable of correcting this disturbed activity and at the same time reduce oedema.
 ...
PMID:[Vasogenic cerebral oedema. Changes in membrane ATPases. Correction by a phospholipid precursor (author's transl)]. 15 43

Previous animal and human studies showed that photic stimulation (PS) increased cerebral blood flow and glucose uptake much more than oxygen consumption, suggesting selective activation of anaerobic glycolysis. In the present studies, image-guided 1H and 31P magnetic resonance spectroscopy (MRS) was used to monitor the changes in lactate and high-energy phosphate concentrations produced by PS of visual cortex in six normal volunteers. PS initially produced a significant rise (to 250% of control, p less than 0.01) in visual cortex lactate during the first 6.4 min of PS, followed by a significant decline (p = 0.01) as PS continued. The PCr/Pi ratios decreased significantly from control values during the first 12.8 min of PS (p less than 0.05), and the pH was slightly increased. The positive P100 deflection of the visual evoked potential recorded between 100 and 172 ms after the strobe was significantly decreased from control at 12.8 min of PS (p less than 0.05). The finding that PS caused decreased PCr/Pi is consistent with the view that increased brain activity stimulated ATPase, causing a rise in ADP that shifted the creatine kinase reaction in the direction of ATP synthesis. The rise in lactate together with an increase in pH suggest that intracellular alkalosis, caused by the shift of creatine kinase, selectively stimulated glycolysis.
J Cereb Blood Flow Metab 1992 Jul
PMID:Effect of photic stimulation on human visual cortex lactate and phosphates using 1H and 31P magnetic resonance spectroscopy. 161 37

The functional importance of membrane hyperpolarization through activation of ATP-sensitive K channels, or activation of the Na,K-ATPase, was investigated for acetylcholine (ACh)-induced relaxation of the rabbit isolated middle cerebral artery (MCA) precontracted with uridine triphosphate. Incubation with glibenclamide (1 microM), a known blocker of ATP-sensitive K channels, or precontraction with a high concentration of KCl (50 mM) had no effect on ACh-induced relaxation. Similarly, inhibition of the Na,K-ATPase with ouabain (10 microM) or incubation with a potassium-free solution had either no or only a small effect on ACh-induced relaxation. In contrast, NG-nitro-L-arginine (NOLAG) (1 to 10 microM), a structural analogue of L-arginine and an inhibitor of nitric oxide synthesis, produced concentration-dependent although apparently noncompetitive inhibition of ACh-induced relaxation. This inhibition was partially reversed by application of L-arginine (100 microM), a putative precursor for nitric oxide synthesis. It is concluded that membrane hyperpolarization induced by activation of ATP-sensitive K channels or Na,K-ATPase does not play a major functional role in ACh-induced relaxation of rabbit MCA. The potent inhibitory actions of NOLAG would suggest that the major mechanism of ACh-induced relaxation is by release of nitric oxide as in other cerebral and peripheral arteries.
J Cereb Blood Flow Metab 1991 Jul
PMID:Analysis of acetylcholine-induced relaxation of rabbit isolated middle cerebral artery: effects of inhibitors of nitric oxide synthesis, Na,K-ATPase, and ATP-sensitive K channels. 164 28

During partial ischemia, sodium and potassium ions exchange across the blood-brain barrier, resulting in a net increase in cations and brain edema. Since this exchange is likely mediated by specific transporters such as Na,K-ATPase in the capillary endothelium and because brain capillary Na,K-ATPase activity is stimulated by increased extracellular potassium in vitro, this study was designed to determine if the rate of blood to brain sodium transport is increased in ischemic tissue having an elevated interstitial fluid potassium concentration ([K]ISF) in vivo. Sprague-Dawley rats were studied between 2-3 h after occlusion of the right middle cerebral artery. To identify where cortical tissue with an elevated [K]ISF could be sampled for transport studies, the regional pattern of cerebral blood flow and [K]ISF was obtained in a group of 17 rats using hydrogen clearance and potassium-selective microelectrode techniques. We observed severely elevated [K]ISF (greater than 10 mM) when CBF was less than 20 ml 100 g-1 min-1 and mildly elevated levels at CBF between 20-45 ml 100 g-1 min-1. In a second group of seven rats, permeability-surface area products (PS products) for 22Na and [3H]alpha-aminoisobutyric acid ([3H]AIB) were determined in ischemic cortex with elevated [K]ISF and in nonischemic cortex. The PS products for AIB were similar in both tissues (2.2 +/- 0.7 and 2.1 +/- 0.4 microliters/g/min) while the PS products for sodium was significantly increased in the ischemic tissue (1.5 +/- 0.2 and 2.4 +/- 1.1 microliters/g/min).(ABSTRACT TRUNCATED AT 250 WORDS)
J Cereb Blood Flow Metab 1991 May
PMID:Blood to brain sodium transport and interstitial fluid potassium concentration during early focal ischemia in the rat. 184 10

Hexachlorocyclohexanes (HCCH) are chlorinated analogs of inositol; the alpha, beta, gamma, and delta isomers of HCCH have the stereochemical configurations of (+/-)-, scyllo-, muco-, and myo-inositol, respectively. To assess their potential as specific tools for the study of agonist-stimulated phosphoinositide metabolism, we examined the effects of these four HCCH isomers on phosphatidylinositol (PI) synthase (CDP-1,2-diacyl-sn-glycerol:myo-inositol 3-phosphatidyltransferase), PI:inositol exchange enzyme, and several membrane-associated enzymes unrelated to inositol metabolism. In pancreas microsomes, in the presence of saturating myo-inositol, the alpha, beta, gamma, and delta isomers (4 mM) inhibited PI synthase activity by 9, 4, 22, and 69%, respectively. Half-maximal inhibition by delta-HCCH occurred at 0.25 mM. A similar pattern of HCCH inhibition was obtained using n-octylglucopyranoside-solubilized and partially purified PI synthase preparations. The inhibition by delta-HCCH was noncompetitive versus myo-inositol. The PI:inositol exchange enzyme in mouse pancreas microsomes was inhibited 90% by 1 mM delta-HCCH in the presence of 0.25% Triton X-100, but not in its absence; half-maximal inhibition occurred with 0.5 mM delta-HCCH. delta-HCCH (4 mM) also inhibited to varying extents the following enzymes: pancreas CDP-choline:1,2-diacyl-sn-glycerol cholinephosphotransferase (75%), brain and erythrocyte (Na+,K+)-ATPase (87 and 70%), brain and erythrocyte Mg2+-ATPase (38 and -5%), brain 1,2-diacyl-sn-glycerol kinase (22%), and liver glucose 6-phosphatase (16%). gamma-HCCH (4 mM) inhibited these enzymes to a lesser extent, or not at all. The order of inhibition by HCCH stereoisomers was the same as the order of their saturation level in phospholipid vesicles (delta greater than gamma greater than alpha greater than beta). This suggests that the inhibitory action is due to insertion of the compounds either into hydrophobic domains of the enzymes or into annular lipid. The results indicate that the HCCHs are not selective inhibitors of inositol metabolism.
 ...
PMID:Inhibition of phosphatidylinositol synthase and other membrane-associated enzymes by stereoisomers of hexachlorocyclohexane. 257 70

The development of transport functions in the rabbit choroid plexus was followed postnatally up to 2 months after birth. The activity of ouabain-sensitive Na+, K+-ATPase in newborn rabbit choroid plexus composes about one-fourth (lateral and third ventricle) to one-half (fourth ventricle) of the activity in the adult animal, and it increases markedly within the first 3 weeks of early life. A similar profile of postnatal changes is observed for the capacity to take up and accumulate the organic base choline, which is about three to five times higher for the adult rabbit than for the newborn animal. This coincides with the maturation of the epithelial cells as well as with the development of the sympathetic nerve supply in the choroid plexus. The results suggest that energy-dependent translocation systems influenced by local sympathetic nerves in the choroid plexus, at the interface between blood and CSF, have a functional role shortly after birth.
J Cereb Blood Flow Metab 1985 Dec
PMID:Early postnatal development of transport functions in the rabbit choroid plexus. 293 54

The energy-dependent transport of ions across the blood-brain barrier and the blood-cerebrospinal fluid barrier by Na+, K+-ATPase is credited with an important role in brain homeostasis. In this study, we have assessed the relative enrichment of Na+, K+-ATPase in regional brain capillary preparations and in the choroid plexus by the quantitative determination of the cardiac glycoside binding sites in these preparations using [3H]ouabain as a ligand. We find that ouabain binds specifically to brain microvessels of the rat and the pig and to the choroid plexus of the pig in a saturable manner. The maximum density of ouabain binding sites in brain microvessels of both species is about one-fourth that of the crude membranes of the cerebrum and cerebellum. The density of ouabain binding sites in the pig choroid plexus is intermediate between that of the brain and brain microvessels. We do not find regional differences in ouabain binding to membrane fractions of the cerebrum and cerebellum, nor any significant differences in ouabain binding to cerebral and cerebellar microvessels. These findings provide quantitative estimates of Na+, K+-ATPase in brain capillaries and choroid plexus.
J Cereb Blood Flow Metab 1985 Mar
PMID:Specific ouabain binding to brain microvessels and choroid plexus. 298 90

A rat brain P3 fraction enriched in ER derived microsomes was centrifuged through a 20-40% linear sucrose gradient in a Beckman Ti-14 Zonal rotor and 11 fractions were obtained. The distribution of marker enzyme activities and protein were determined in these 11 subfractions. NADPH-Cytochrome C reductase, choline phosphotransferase were employed for endoplasmic reticulum, Na+,K+-ATPase, 5'-nucleotidase, and acetylcholinesterase were employed for plasma membrane, 2',3'-cyclic nucleotide phosphohydrolase was employed for myelin. The bulk of the protein was recovered in the 24-34% sucrose fractions, Na+,K+-ATPase, 5'-nucleotidase, and acetylcholinesterase were in the 22-38% sucrose fractions while NADPH-cytochrome C reductase and CNPase were enriched in the 20-22% sucrose fractions. The ethanolamine and the serine base exchange activities had a bimodal distribution, with highest specific activities in sucrose fractions 32-34% and 20-24%. Choline base exchange activity was nearly undetectable in all the fractions. The specific activities of CDP-choline phosphotransferase, and phospholipid-N-methyltransferase were highest in the 20-22% sucrose fraction. Phospholipid-N-methyltransferase activity was significantly stimulated in the presence of exogenous phospholipid acceptors as phosphatidylethanolamine or phosphatidylmonomethylethanolamine or phosphatidyldimethylethanolamine, however, the greatest response was with phosphatidylmonomethylethanolamine. The rat brain P3 fraction yielded a population of a membrane at the light end of the sucrose gradient which has a buoyant density similar to myelin but seemed to be enriched with NADPH cytochrome C reductase and phospholipid modifying enzymes. This is in contrast to liver microsomes submitted to a similar fractionation.
 ...
PMID:Distribution of selected phospholipid modifying enzymes in rat brain microsomal subfractions prepared by density gradient zonal rotor centrifugation. 298 22

The role of endogenous cerebral norepinephrine (NE) as a modulator of transmembrane cation transport and energy metabolism was evaluated by monitoring extracellular potassium ion activity ([K+[o) in vivo and by measuring cortical Na+,K+-ATPase activity and oxygen consumption in vitro. Ipsilateral cortical NE was depleted by unilateral 6-hydroxydopamine (6-OHDA) lesions of the locus ceruleus (LC). The contralateral cortex was used for control measurements. NE depletion had no effect on resting levels of cortical [K+[o or on the rate of K+ removal from the extracellular space following direct cortical stimulation. There was also no effect of NE depletion on Na+,K+-ATPase activity in cortical homogenates nor on oxygen consumption of cortical slices over a wide range of K+ concentrations. These results indicate tht central NE depletion does not influence movements of cortical K+ either directly through an influence on Na+,K+-ATPase activity or indirectly through effects on oxidative metabolism. It is probable, therefore, that previously described effects of NE on cortical oxidative metabolism are mediated through changes in cerebral perfusion and/or modification of substrate availability in vivo.
J Cereb Blood Flow Metab 1982 Sep
PMID:Does endogenous norepinephrine regulate potassium homeostasis and metabolism in rat cerebral cortex? 628 73

This study documents the Na+,K+-ATPase activity as well as selected parameters of oxidative metabolism and electrophysiological function in rat brain exposed to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. During a 0.5-h ischemic exposure in which the electroencephalograph (EEG) was abolished and energy metabolism severly compromised the Na+,K+-ATPase showed a capability for enhanced activity (120-140% of control). On recirculation, the Na+,K+-ATPase activity showed a phasic pattern, which was characterized by normal values at 0.25-2 h, increased values (115-125% of control) at 3-24 h, and, finally, normal values at 72 h of recirculation, respectively. The maintenance of Na+,K+-ATPase integrity was correlated with a gradual return of EEG activity and virtually complete restitution of the cerebral energy state during the 72 h of recirculation. Measurements of thiobarbituric acid reactive material and water soluble antioxidant during ischemia and recirculation gave no evidence of the presence of significant free radical lipid peroxidation in this model. It is concluded that Na+,K+-ATPase and its associated membrane lipids are not irreversibly damaged by ischemia in which the tissue lactacidosis is limited to less than 20 mumol g-1.
J Cereb Blood Flow Metab 1982 Dec
PMID:Cerebral Na+,K+-ATPase activity during exposure to and recovery from acute ischemia. 629 42


1 2 3 4 Next >>