Potassium and Calcium Channels

Abstract

K channels are present in all the cells and maintain resting membrane potentials. Closing of K channel leads to depolarisation.

• Voltage-gated K channels: get activated by the change in cell membrane potential. Twelve different subtypes are seen (Kiv1–Kiv12). Nerve injury decreases K currents causing hyperalgesia. 4-Aminopyridine and tetraethylammonium can block voltage-gated K channels. Prostaglandins mediate their analgesic effects through voltage-gated K channels.

• Calcium-activated K channels: they are divided into three families:

  • Large conductance

  • Intermediate conductance

  • Small conductance

  All of these are activated when cytoplasmic concentration of calcium is increased.

• Inwardly rectifying K channels: they alter the direction of ionic flow. They facilitate influx more than the efflux. They are further divided into seven families (Kiv1–Kiv7). Gir 3(G-protein-regulated inwardly rectifying K channel) is involved with nociception.

• Adenosine triphosphate-sensitive K channel (KATP/Kiv6): found in muscles, neurons and pancreas. This channel is involved with morphine-induced antinociception.

• KCNQ K channels (Km or Kiv7 channels): mutations of this channel result in human diseases. They produce M current (blocked by muscarinic agonists) and are voltage gated. They are present in sensory neurons and have an important role in analgesia. Drugs acting on this channel include retigabine, flupirtine and linopirdine.

• Two-pore domain K channels: widely distributed and have a role in the action of local anaesthetics and have a role in the control of the resting membrane potential.