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NITRIC OXIDE DOES NOT MEDIATE PROMOTION OF CELLULAR POTASSIUM RELEASE BY PHENOLPHTHALEIN IN COS‐7 CELLS
Author(s) -
Mason Robert W,
Hopp Laszlo,
Lloyd John B
Publication year - 2004
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2004.03989.x
Subject(s) - phenolphthalein , chemistry , nitric oxide , potassium , sodium nitroprusside , nitric oxide synthase , biochemistry , organic chemistry
SUMMARY 1. It has been proposed that phenolphthalein exerts its laxative effect via an intracellular cascade that begins with the activation of nitric oxide synthase (NOS) and ends with an inhibition of NaCl and water reabsorption from the colon. Phenolphthalein also promotes the release of potassium from cells, but it is not known how this is related to its effect on sodium and water uptake. 2. An established in vitro system was used to examine the role of nitric oxide (NO) in phenolphthalein‐induced release of 86 Rb + from COS‐7 cells. 3. Sodium nitroprusside, an NOS‐independent NO source, was unable to mimic the effects of phenolphthalein and N G ‐nitro‐ l ‐arginine methyl ester, an NOS inhibitor, was unable to block the effect of phenolphthalein. 4. It is concluded that NO generation is not required for phenolphthalein‐stimulated potassium release. It is proposed that the effect of phenolphthalein on cellular potassium release is mechanistically distinct from the effect on NaCl and water uptake by colonocytes.