Related Experiment Video
Updated: Jun 14, 2026

Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique
Published on: February 7, 2025
Bisphenol A activates Maxi-K (K(Ca)1.1) channels in coronary smooth muscle
Shinichi Asano1, Johnathan D Tune, Gregory M Dick
1Division of Exercise Physiology, Center for Cardiovascular & Respiratory Sciences, West Virginia University School of Medicine, Morgantown, WV, USA.
Background And Purpose:
Bisphenol A (BPA) is used to manufacture plastics, including containers for food into which it may leach. High levels of exposure to this oestrogenic endocrine disruptor are associated with diabetes and heart disease. Oestrogen and oestrogen receptor modulators increase the activity of large conductance Ca(2+)/voltage-sensitive K(+) (Maxi-K; K(Ca)1.1) 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 beta1 subunit.
Experimental Approach:
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 alpha or alpha plus beta1 subunits.
Key Results:
BPA (10 microM) activated an outward current in smooth muscle cells that was inhibited by penitrem A (1 microM), 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 alpha subunits alone, 10 microM BPA did not affect channel activity. When channels in AD-293 cells contained beta1 subunits, 10 microM BPA increased channel activity. Effects of BPA were rapid (<1 min) and reversible. A higher concentration of BPA (100 microM) increased Maxi-K current independent of the beta1 subunit.
Conclusions And Implications:
Our data indicate that BPA increased the activity of Maxi-K channels and may represent a basis for some potential toxicological effects.
Related Concept Videos
Antihypertensive Drugs: Action of Calcium Channel Blockers
G-Protein Gated Ion Channels
Sensory organs,...
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Antihypertensive Drugs: Vasodilators
Nitric Oxide Signaling Pathway
Adrenergic Receptors: β Subtype
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...

