Large-conductance calcium-activated potassium channels
(also known as maxi-K or BK channels) play a pivotal role
in modulating vasomotor tone in both health and disease. BK
channels, expressed on VSMCs, act as breaks for the increase
in vascular tone that occurs after membrane depolarization and
elevation of cytosolic calcium. An intracellular rise in cytosolic
calcium through VDCC leads to activation of ryanodine
receptors that release quanta of calcium from the sarcoplasmic
reticulum (calcium sparks). It is these intracellularly generated
sparks that elevate local submembrane concentrations of
calcium and activate BK channels which increase potassium
conductance and lower membrane potential.1
This reduces
opening of VDCCs, thus modulating contraction (Figure2
).