Ion channels and receptor-mediated Ca2+ influx in neutrophil granulocytes.
Although generally classified as non-excitable cells, human neutrophils possess a variety of ion channels that play a crucial role in the regulation of cellular activity. The mechanism of receptor-mediated Ca2+ influx in neutrophils is complex. Receptor agonists empty intracellular Ca2+ stores via generation of Ins(1,4,5)P3. The emptying of intracellular Ca2+ stores leads by an hitherto not understood mechanism to the activation of Ca2+ influx across the plasma membrane. Neutrophils possess at least 2 types of K+ channels. Voltage-activated K+ channels, important for the maintenance of the resting potential, and Ca2+ activated K+ channels, important for the repolarization after cellular activation. Neutrophils also possess voltage- and pH activated H+ channels that serve to extrude protons, generated by the neutrophil respiratory burst. Neutrophils depolarize in response to activation by agonists. The mechanism of neutrophil depolarization involves electron transport by the respiratory burst oxidase. Neutrophil depolarization serves as a negative feed-back mechanism, it also activates the H+ channels and thereby stimulates extrusion of protons.
Krause
K H
KH
Division of Infectious Diseases, University Hospital, Geneva, Switzerland.
Demaurex
N
N
Jaconi
M
M
Lew
D P
DP
D002118:Calcium / Q000378:metabolism*; D005246:Feedback; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000502:physiology; D015640:Ion Channel Gating; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008564:Membrane Potentials; D009504:Neutrophils / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011522:Protons; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D014407:Tumor Cells, Cultured
D007473:Ion Channels; D011522:Protons; D011956:Receptors, Cell Surface; D015544:Inositol 1,4,5-Trisphosphate; D011188:Potassium; D002118:Calcium