Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of polyunsaturated fatty acids on brain edema formation have been studied in rats. Intracerebral injection of polyunsaturated fatty acids (PUFAs), including linolenic acid (18:3) and arachidonic acid (20:4), caused significant increases in cerebral water and sodium content concomitant with decreases in potassium content and Na+- and K+- dependent adenosine triphosphatase activity. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acid were not effective in inducing brain edema. The [125I]-bovine serum albumin spaces increased twofold and threefold at 24 hours with 18:3 and 20:4, respectively, indicating vasogenic edema with increased permeability of brain endothelial cells. Staining of the brain was observed five minutes after injection of Evans blue dye followed by arachidonic acid perfusion. A major decrease in brain potassium content was evidence of concurrent cellular (cytotoxic) edema as well. The induction of brain edema by arachidonic acid was dose dependent and maximal between 24 and 48 hours after perfusion. Dexamethasone (10 mg/kg) was effective in ameliorating the brain edema, whereas a cyclooxygenase inhibitor, indomethacin (10 mg/kg), was not. These data indicate that arachidonic acid and other PUFAs have the ability to induce vasogenic and cellular brain edema and further support the hypothesis that the degradation of phospholipids and accumulation of PUFAs, particularly arachidonic acid, initiate the development of brain edema in various disease states.
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PMID:Induction of brain edema following intracerebral injection of arachidonic acid. 630 72

We studied the role of sodium ions in mediating basal and stimulated ACTH release from perifused rat anterior pituitary cells by exposing the cells to the sodium channel opener veratridine or the Na+/K(+)-adenosine triphosphatase inhibitor ouabain to increase the intracellular Na+ concentration or, conversely, by omitting Na+ from the perifusion medium or blocking Na+ entry into the cell with tetrodotoxin, a voltage-dependent sodium channel blocker, to decrease the intracellular Na+ concentration. Neither tetrodotoxin nor Na(+)-free medium had a significant effect on 100 nM arginine vasopressin (AVP) or 10 nM ovine corticotropin-releasing hormone (CRH)-induced ACTH secretion. Veratridine increased basal ACTH secretion by 122% (41.3 +/- 2.9 vs. 18.6 +/- 0.4 pg/min; P < 0.001), the initial spike phase of the response to AVP by 65% (0.28 +/- 0.01 vs. 0.17 +/- 0.03 ng/3 min; P < 0.005), the subsequent sustained phase to AVP by 129% (0.16 +/- 0.01 vs. 0.07 +/- 0.01 ng/7 min; P < 0.005), and the total response to CRH by 70% (0.39 +/- 0.01 vs. 0.23 +/- 0.04 ng/10 min; P < 0.05). Ouabain increased basal ACTH secretion by 39% (45.7 +/- 2.8 vs. 32.9 +/- 2.1 pg/min; P < 0.05), the initial spike phase of the response to AVP by 88% (0.32 +/- 0.02 vs. 0.17 +/- 0.01 ng/3 min; P < 0.005), the sustained phase response to AVP by 67% (0.10 +/- 0.01 vs. 0.06 +/- 0.01 ng/7 min; P < 0.05), and the total integrated response to CRH by 49% (0.88 +/- 0.09 vs. 0.59 +/- 0.03 ng/10 min; P < 0.05). However, the effects of both veratridine and ouabain on basal ACTH secretion were significantly attenuated in Ca(2+)-free EGTA-containing medium, suggesting that this effect was indirect, due to membrane depolarization and consequent influx of extracellular Ca2+. Dexamethasone (100 nM) had no effect on the ACTH response to either veratridine or ouabain. We conclude that changes in the intracellular Na+ concentration and sodium channel activity are not directly involved in AVP- or CRH-induced ACTH secretion.
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PMID:The role of sodium in mediating adrenocorticotropin secretion by perifused rat anterior pituitary cells. 778 18

Glucocorticoids have been reported to aggravate ischemic neuronal damage. Because energy failure is a crucial factor in the development of ischemic neuronal injury, the effects of dexamethasone on histologic outcome and energy metabolism were investigated in gerbil brain. Dexamethasone (3 microg, i.c.v.) was administered 1 h prior to ischemia, and its effect on delayed neuronal death caused by 2 min of bilateral common carotid artery occlusion was observed in hippocampal CA1 pyramidal neurons. The brain concentration of ATP after various durations of decapitation ischemia was determined, and the effect of dexamethasone (3 microg, i.c.v.) was examined. Na+,K+-activated adenosine triphosphatase (Na+,K+-ATPase) activity was evaluated after the administration of the agent. Forebrain ischemia for 2 min produced neuronal damage in animals pretreated with dexamethasone, although neuronal damage was not observed in vehicle-injected animals. Decapitation ischemia for 0.5 and 1 min reduced the brain ATP concentration to 44% and 15% of the basal level, respectively. Dexamethasone attenuated the ischemia-induced reduction in ATP, and the values were 58% and 25% of the basal level, respectively. Na+,K+-ATPase activity at pH 6.7 was suppressed to 47% by dexamethasone treatment (3 microg, i.c.v.), whereas the activity at pH 7.4 was not influenced by the agent. The results show that a contributing factor to the aggravation of ischemic neuronal damage may be a disturbance in Na+,K+-ATPase despite adequate levels of ATP.
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PMID:Dexamethasone reduces energy utilization in ischemic gerbil brain. 1155 63