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Reinvestigation of drugs and chemicals as aquaporin-1 inhibitors using pressure-induced hemolysis in human erythrocytes.

Abstract
Recently, we have found that pressure-induced hemolysis is enhanced by inhibiting water transport via aquaporin-1 (AQP1), as seen in p-chloromercuribenzoate (pCMB)-treated erythrocytes. So, using this method we reinvestigated the functions as AQP1 inhibitors of drugs and chemicals such as acetazolamide, sodium nitroprusside, tetraethylammonium ions (TEA(+)), and dimethylsulfoxide (DMSO). The values of hemolysis at 200 MPa were almost unaffected by acetazolamide or sodium nitroprusside, decreased by TEA(+), and increased significantly by DMSO. Furthermore, the erythrocytes were exposed to pCMB in the presence of TEA(+) or DMSO. The enhancement effect of pCMB on pressure-induced hemolysis was unaffected by TEA(+) but attenuated by DMSO. Taken together, these results suggest that, of drugs and chemicals examined here, DMSO only is an AQP1 inhibitor, but the effect of DMSO is small compared with pCMB.
AuthorsTakeo Yamaguchi, Yohei Iwata, Shingo Miura, Kazumasa Kawada
JournalBiological & pharmaceutical bulletin (Biol Pharm Bull) Vol. 35 Issue 11 Pg. 2088-91 ( 2012) ISSN: 1347-5215 [Electronic] Japan
PMID23123479 (Publication Type: Journal Article)
Chemical References
  • Aquaporin 1
  • Nitroprusside
  • p-Chloromercuribenzoic Acid
  • Tetraethylammonium
  • Acetazolamide
  • Dimethyl Sulfoxide
Topics
  • Acetazolamide (pharmacology)
  • Aquaporin 1 (antagonists & inhibitors)
  • Cells, Cultured
  • Dimethyl Sulfoxide (pharmacology)
  • Erythrocytes (drug effects, physiology)
  • Hemolysis (drug effects)
  • Humans
  • Nitroprusside (pharmacology)
  • Pressure
  • Tetraethylammonium (pharmacology)
  • p-Chloromercuribenzoic Acid (pharmacology)

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