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Bisphenol A activates Maxi‐K channels in coronary smooth muscle
Author(s) -
Asano Shinichi,
Dick Gregory M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.986.2
Subject(s) - bisphenol a , myocyte , chemistry , patch clamp , endocrinology , conductance , biophysics , electrophysiology , medicine , estrogen , endocrine disruptor , biology , biochemistry , hormone , endocrine system , mathematics , organic chemistry , combinatorics , epoxy
Bisphenol A (BPA) is used to manufacture plastics, including food containers into which it leaches. Exposure to this estrogenic endocrine disruptor is associated with diabetes and heart disease. Estrogen and estrogen receptor modulators increase the activity of large conductance Ca 2+ /voltage‐sensitive K + (Maxi‐K) channels, but the effects of BPA on Maxi‐K channels are unknown. We tested the hypothesis that BPA activates Maxi‐K channels through a mechanism that depends upon the regulatory β1 subunit. Patch clamp recordings of Maxi‐K channels were made in human and canine coronary smooth muscle cells as well as in AD‐293 cells expressing pore‐forming α or α plus β1 subunits. BPA (10 μM) activated an outward current in smooth muscle cells that was inhibited by penitrem A (1 μM), a Maxi‐K blocker. BPA increased Maxi‐K activity in inside‐out patches from coronary smooth muscle, but had no effect on single channel conductance. In AD‐293 cells with Maxi‐K channels composed of α subunits alone, 10 μM BPA did not affect channel activity. When channels in AD‐293 cells contained β1 subunits, 10 μM BPA increased channel activity. Effects of BPA were rapid (<1 min) and reversible. A higher concentration of BPA (100 μM) increased Maxi‐K current independent of the β1 subunit. These data indicate BPA increases the activity of Maxi‐K channels and may represent a basis for some potential toxicological effects.