Bisphenol A activates Maxi-K (KCa1.1) channels in coronary smooth muscle

摘要: Background and purpose:  Bisphenol A (BPA) is used to manufacture plastics, including containers for food into which it may leach. High levels of exposure this oestrogenic endocrine disruptor are associated with diabetes heart disease. Oestrogen oestrogen receptor modulators increase the activity large conductance Ca2+/voltage-sensitive K+ (Maxi-K; KCa1.1) channels, but effects BPA on Maxi-K channels unknown. We tested hypothesis that activates through a mechanism depends upon regulatory β1 subunit. Experimental approach:  Patch-clamp recordings were made in human canine coronary smooth muscle cells as well AD-293 expressing pore-forming α or plus subunits. Key results:  (10 µM) activated an outward current was inhibited by penitrem (1 µM), blocker. increased inside-out patches from muscle, had no effect single channel conductance. In composed subunits alone, 10 µM did not affect activity. When contained subunits, Effects rapid (<1 min) reversible. higher concentration (100 µM) independent subunit. Conclusions implications:  Our data indicate represent basis some potential toxicological effects.