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Potassium transporters: outward current


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Potassium transporters: outward current

Regulation of outward potassium current

Potassium currents play vital role in functioning of all excitable systems. Outwardpotassium currents are mediated by different types of channels and support differentphysiological functions depending on the expressing tissue. Potassium flow out of thecell generally leads to hyperpolarization and reduction of cell excitability.

Superfamily of voltage-gated potassium channels (Kv) is the largest group of proteinsthat mediate transmembraneous potassium flow. The superfamily of Kv-alpha subunits can besubdivided into three major families. The first family is represented by Shaker-relatedKv-alpha subunits (Kv1.x....Kv9.x), the second by ether-a-go-go-related Kv-alpha subunits(KCNH), and the third one KCNQ-related Kv-alpha subunits. Kv subunits can formheteromultimers as well as complexes with various auxiliary subunits [1],[2]. For example, KQT-like family (KCNQ) of potassium voltage-gated channelsplay important role in the heart, inner ear, and the intestine. A product of KCNQ1gene co-assembles with Potassium voltage-gated channel Isk-related family member 3 (KCNE3 ) subunit in the crypt cells of the small intestine and colon. PotassiumKCNQ1 + KCNE3 current appears to play an important role in intestinalchlorine homeostasis, which is altered in conditions such as cystic fibrosis and cholera.KCNQ1 is also implicated in the functioning of the inner ear. KCNQ1co-assembles here, as in the heart, with KCNE1 to form functional channels.Mutations in both KCNQ1 and KCNE1 may lead to deafness and vestibulardisturbance. KCNQ2, KCNQ3, and possibly KCNQ5 are involved in thewidely neuronally distributed potassium M-current [3].

Potassium inwardly rectifying channels which includes seven subfamilies: Kir1.x, Kir2.x, GIRK, Kir 4.x, Kir5.x, Kir 6.x, Kir 7.x channels control the restingpotential and the input

resistance of a cell and yet allow action potential generation and prolongeddepolarization of cell membrane once the membrane is sufficiently depolarized.[4].

G protein-activated inward rectifier potassium ( GIRK ) channels regulate theheart rate and the neuronal activity by neurotransmitters, and are the only ion channelsconclusively shown to be activated by a direct interaction with heterotrimeric G proteinsubunits [5].

Kir 6.x, together with ATP-binding cassette sub-family C member 8/9 ( SUR1/SUR2 ) subunits, forms ATP-sensitive potassium channels. When expressed inbeta-cells, Kir6.x channels play a key role in the regulation of insulin secretion inresponse to changes in glucose metabolism. Opening of cardiac Kir6.x channels is thoughtto protect against myocardial damage from ischemia. In endothelial cells, Kir 6.xchannels serve as a regulators of the resting potential during energy impairment, and maymodulate the release of endothelium-derived relaxing factor under such conditions [6], [7].

Outward potassium currents can be activated by various stimuli including rise ofintracellular calcium concentration. Three broad families of calcium-activated potassiumchannels have been identified up to date. These are Potassium large conductancecalcium-activated channel (including Potassium large conductance calcium-activatedchannel, subfamily M alpha member 1 ( MaxiK alpha ), Potassium small conductancecalcium-activated channels ( SK1, SK2, SK3 ) and Potassiumintermediate conductance calcium-activated channels ( SK4/IK1 ). Calcium-activatedpotassium currents are known to mediate different phases of after hyperpolarization(coming after action potential) in neurons [8].