Their function is to repolarize the membrane potential by allowing for potassium to flow outward, in response to a depolarization or increase in calcium levels.

[5] The VSD associates with the PGD via three major interactions: BK channels are associated and modulated by a wide variety of intra- and extracellular factors, such as auxiliary subunits (β, γ), Slobs (slo binding protein), phosphorylation, membrane voltage, chemical ligands (Ca²⁺, Mg²⁺), PKC, The BK α-subunits assemble 1:1 with four different auxiliary types of β-subunits (β1, β2, β3 or β4).

[10] Trafficking to and expression of BK channels in the plasma membrane has been found to be regulated by distinct splicing motifs located within the intracellular C-terminal RCK domains.

In particular a splice variant that excluded these motifs prevented cell surface expression of BK channels and suggests that such a mechanism impacts physiology and pathophysiology.

The CTD activates the BK channel when bound with intracellular Mg²⁺ to allow for interaction with the voltage sensor domain (VSD).

[5] Energy provided by voltage, Ca²⁺, and Mg²⁺ binding will propagate to the activation gate of BK channels to initiate ion conduction through the pore.

[13] Various γ subunits during early brain development are involved in neuronal excitability and in non-excitable cells they often are responsible as a driving force of calcium.

[10] There is further evidence that inhibiting BK channels would prevent the efflux of potassium and thus reduce the usage of ATP, in effect allowing for neuronal survival in low oxygen environments.

[10] BK channels can also function as a neuronal protectant in terms such as limiting calcium entry into the cells through methionine oxidation.

Slo binding proteins (Slobs) can modulate BK channels as a function of circadian rhythms in neurons.

[10] Mutations of BK channels, resulting in a lower amount of expression in mRNA, is more common in people who have mental disabilities (via hypofunction [15]), schizophrenia or autism.

[10] Moreover, increased repolarization caused by BK channel mutations may lead to dependency of alcohol initiation of dyskinesias, epilepsy or paroxysmal movement disorders.

[10] Not only are BK channels important in many cellular processes in the adult it also is crucial for proper nutrition supply to a developing fetus.

[10] However, increased expression of BK channels have been found in tumor cells, and this could influence future cancer therapy, discussed more in the pharmacology section.

BK channels can be activated by exogenous pollutants and endogenous gasotransmitters carbon monoxide,[16][17] nitric oxide, and hydrogen sulphide.

[14] It is known that BK channels do in some way influence the division of cells during replication, which when unregulated can lead to cancers and tumors.

BK channels can be used as pharmacological targets for the treatment of several medical disorders including stroke[19] and overactive bladder.

For instance, BMS-204352, a molecule developed by Bristol-Myers Squibb, failed to improve clinical outcome in stroke patients compared to placebo.

[22] However, there have been some success from the agonist to BKCa channels, BMS-204352, in treating deficits observed in Fmr1 knockout mice, a model of Fragile X syndrome.

There has been research displaying that a blockage of BK channels results in an increase in neurotransmitter release, effectively indicating future therapeutic possibilities in cognition enhancement, improved memory, and relieving depression.

Oxidative stress on BK channels can lead to the negative impairments of lowering blood pressure through cardiovascular relaxation have on both aging and disease.

[10] Thus, the signaling system can be involved in treating hypertension and atherosclerosis[10] through targeting of the ɑ subunit to prevent these detrimental effects.