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

The effect of membrane excitability on (Na+ + K+)-adenosine triphosphatase (ATPase) was studied in rat brain slices. The treatment of the brain cortical slices with veratrine for more than 10 min caused a significant decrease of the (Na+ + K+)-ATPase activity. The similar inhibition of the enzyme by veratrine was observed in the hippocampus and hypothalamus, and the veratrine treatment did not affect the sensitivity of the cortical enzyme for ouabain inhibition. These findings suggest that two isozymes of (Na+ + K+)-ATPase are equally inhibited by the treatment. Veratrine inhibited the partial reactions such as Na+-dependent phosphorylation and K+-stimulated phosphatase as well as the specific binding of [3H]ouabain. Agents which increase intracellular Na+ concentration also inhibited the enzyme activity. The effects of veratrine were blocked by Na+-free medium or tetrodotoxin. Low Na+ medium decreased the enzyme activity, and the effect was blocked by amiloride or Ca++-free medium, indicating the involvement of Na+/Ca++ exchange in the inhibition. The decreased activity induced by low Na+ or high K+ medium was restored to the normal level by the subsequent incubation in normal medium. The inhibitory effect of veratrine was dependent on external Ca++, and was blocked by addition of W-7 [N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide]. A23187 also decreased (Na+ + K+)-ATPase activity in the slices. High Mg++ medium blocked the effect of veratrine but not that of monensin which was not dependent on external Ca++.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Veratrine-induced decrease of (Na+ + K+)-adenosine triphosphatase activity in rat brain slices. 253 13

Isolated atria of guinea-pigs were treated with veratrine until the initial signs of toxicity were seen. Ouabain was then added cumulatively, starting with a threshold inotropic concentration, 50 nM, until the tissue became dysrhythmic. It was found that a concentration of ouabain which by itself gave a positive inotropic effect of only 3%, significantly enhanced the toxicity of veratrine. Veratrine had no effect on the (Na+ + K+)-adenosine triphosphatase ((Na+ + K+)-ATPase) enzyme isolated from guinea-pig ventricle. The conclusion drawn is that at threshold inotropic concentrations of ouabain it is likely that the (Na+ + K+)-ATPase is inhibited rather than stimulated.
 ...
PMID:Enhancement of the toxic effects of veratrine on guinea-pig atrium by threshold inotropic doses of ouabain. 624 31

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.
 ...
PMID:The role of sodium in mediating adrenocorticotropin secretion by perifused rat anterior pituitary cells. 778 18