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Chemical Compound Review

EIPA     3-amino-6-chloro-N- (diaminomethylidene)-5...

Synonyms: Lopac-A-3085, CHEMBL517986, AG-J-19240, A3085_SIGMA, CHEBI:606573, ...
 
 
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Disease relevance of Ethylisopropylamiloride

  • These findings are consistent with short-term exposure to EIPA accelerating ATP depletion during ischemia, as well as limiting proton efflux during reperfusion [1].
  • 6. In CO2-HCO3(-)-buffered Tyrode solution, pHi recovery from an intracellular acidosis (NH4+ pre-pulse) was only partially inhibited by EIPA or amiloride whereas Nao+ removal completely inhibited the recovery [2].
  • OBJECTIVE: The aim was to investigate the effect of ethylisopropylamiloride (EIPA), an inhibitor of Na+/H+ exchange, and of extracellular pH on the proliferation of immortalised lymphoblasts derived from patients with essential hypertension and normotensive controls [3].
  • Addition of 1 x 10(-5) mol/l amiloride or 3 x 10(-7) mol/l 5-(N-ethyl-N-isopropyl)amiloride (EIPA) markedly decreased the incidence and duration of ventricular fibrillation or even suppressed fibrillation completely as in the case of 1 x 10(-6) mol/l EIPA [4].
  • 3. Release is also enhanced by lignocaine but inhibited by amiloride and ethylisopropylamiloride, suggesting that sodium entry into adrenergic nerve terminals during anoxia occurs by Na+/H+ (and possibly Na+/Ca2+) exchange [5].
 

High impact information on Ethylisopropylamiloride

 

Chemical compound and disease context of Ethylisopropylamiloride

 

Biological context of Ethylisopropylamiloride

 

Anatomical context of Ethylisopropylamiloride

 

Associations of Ethylisopropylamiloride with other chemical compounds

 

Gene context of Ethylisopropylamiloride

  • Further, exposure of the cells to GM-CSF, IL-3, or TPA results in sustained pHi alkalinizatio, which is abrogated when the cells are preincubated with 5-(N-ethyl-N-isopropyl)amiloride, a specific inhibitor of the antiport [30].
  • At a maximum noncytotoxic concentration (25 microM), the potent amiloride analog, 5-(N-ethyl-N-isopropyl)amiloride (EP-Am), decreased but did not abolish, the stimulatory effect of hPRL [31].
  • ET-1- but not PMA-stimulated K+ uptake was inhibited by 5-(N-ethyl-N-isopropyl)amiloride (inhibitor of Na+/H+ exchange system), suggesting a linkage of Na+/H+ exchange with ET-1-stimulated Na+,K(+)-ATPase and Na(+)-K(+)-Cl- cotransport activity that is not mediated by PKC [32].
  • Cytosolic pH (pHi) was significantly higher in GLUT1 than LacZ cells, an effect abolished in the presence of Na+/H+ exchange inhibitor ethylisopropylamiloride (1 micromol/L) [33].
  • When the tubules of the WT mice were exposed to the hyperosmotic solution including either of the two P-gp inhibitors, in the absence of peritubular Na+ or in the presence of peritubular ethylisopropylamiloride (EIPA; the specific inhibitor of Na+/H+ exchange), they did not exhibit RVI [34].
 

Analytical, diagnostic and therapeutic context of Ethylisopropylamiloride

References

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