Sodium Potassium Pump's role in Breathing?

  • #1

Main Question or Discussion Point

Hello, this is a question that popped into my head, but I cannot seem to find much literature pertaining to what I am wanting to know.

Does Na+/K+ pump play a role in breathing in humans? If it does, would failure of this pump lead to asphyxiation? If it doesn't, then what DOES play a role in breathing at the cellular level? I am trying to explain how hanging oneself occurs from a biological/neuroscience perspective. I know hypoxia occurs, but I want to go more in-depth to the individual cellular mechanisms/actions that lead to this hypoxia.

Thanks.
 

Answers and Replies

  • #2
BillTre
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Assuming you are talking about the role of the Na+/K+ pump plays in the mechanism of breathing involving both muscle contraction and the the conduction of nerve impulses that drive the contractions,
then the Na+/K+ pump is involved in maintaining the membrane potentials of the nerve and muscle cells.
They will not work right if they don't have the proper membrane potentials.

Not clear how exactly you want to relate this to hanging which (as I understand) can cause death from a broken neck (presumably lack of control of the breathing muscles) or from strangulation, which cuts off blood flow to the brain, resulting in loss of brain activity (and therefore breathing).
 
  • #3
berkeman
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I am trying to explain how hanging oneself occurs from a biological/neuroscience perspective. I know hypoxia occurs, but I want to go more in-depth to the individual cellular mechanisms/actions that lead to this hypoxia.
Why are you asking specifically about hanging? Why not all events that lead to hypoxia? What is your medical background, and what has motivated this question? Thanks.
 
  • #4
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Hanging is mechanical, as is the asphyxia that results therefrom (whether by spinal cord severance, strangulation, suffocation, or some combination thereof) and rapidly progressive hypoxia (complete within minutes) is part of the sequelae of the associated radical apnea (complete discontinuation of breathing). At the cellular level, sodium and potassium are both necessary for keeping the heart beating (as is oxygen). (abstract + preview) ref: https://link.springer.com/chapter/10.1007/978-1-4615-1061-1_18
 
  • #5
Andy Resnick
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Does Na+/K+ pump play a role in breathing in humans?
As mentioned previously, Na-K-ATPase maintains the cell membrane potential and is often referred to as the 'cell's battery', as it's function is required to maintain normal transport of (nearly) *everything* into and out of the cell. Oubain inhibits Na-K-ATPase and quickly results in cell death- hypoxic conditions do not (AFAIK) alter Na-K-ATPase function.

So, Na-K-ATPase does play a role in breathing, because the various cells need to be alive in order to: move the diaphragm, perform gas exchange in the lung, etc. etc.
 
  • #6
atyy
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Oubain inhibits Na-K-ATPase and quickly results in cell death
Oubain does inhibit the Na-K-ATPase. However, it is not clear to me that inhibiting the Na-K-ATPase quickly results in cell death. Do you have a reference for that?
 
  • #7
atyy
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Does Na+/K+ pump play a role in breathing in humans? If it does, would failure of this pump lead to asphyxiation? If it doesn't, then what DOES play a role in breathing at the cellular level? I am trying to explain how hanging oneself occurs from a biological/neuroscience perspective. I know hypoxia occurs, but I want to go more in-depth to the individual cellular mechanisms/actions that lead to this hypoxia.
During ischemia, extracellular glutamate rises, triggering processes that lead to cell death.
Glutamate rises mainly by reverse glutamate transport.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC25876/
The extracellular glutamate concentration ([glu](o)) rises during cerebral ischemia, reaching levels capable of inducing delayed neuronal death. The mechanisms underlying this glutamate accumulation remain controversial. We used N-methyl-D-aspartate receptors on CA3 pyramidal neurons as a real-time, on-site, glutamate sensor to identify the source of glutamate release in an in vitro model of ischemia. Using glutamate and L-trans-pyrrolidine-2,4-dicarboxylic acid (tPDC) as substrates and DL-threo-beta-benzyloxyaspartate (TBOA) as an inhibitor of glutamate transporters, we demonstrate that energy deprivation decreases net glutamate uptake within 2-3 min and later promotes reverse glutamate transport. This process accounts for up to 50% of the glutamate accumulation during energy deprivation. Enhanced action potential-independent vesicular release also contributes to the increase in [glu](o), by approximately 50%, but only once glutamate uptake is inhibited. These results indicate that a significant rise in [glu](o) already occurs during the first minutes of energy deprivation and is the consequence of reduced uptake and increased vesicular and nonvesicular release of glutamate.

https://www.ncbi.nlm.nih.gov/pubmed/10659851
The release of glutamate during brain anoxia or ischaemia triggers the death of neurons, causing mental or physical handicap. The mechanism of glutamate release is controversial, however. Four release mechanisms have been postulated: vesicular release dependent on external calcium or Ca2+ released from intracellular stores; release through swelling-activated anion channels; an indomethacin-sensitive process in astrocytes; and reversed operation of glutamate transporters. Here we have mimicked severe ischaemia in hippocampal slices and monitored glutamate release as a receptor-gated current in the CA1 pyramidal cells that are killed preferentially in ischaemic hippocampus. Using blockers of the different release mechanisms, we demonstrate that glutamate release is largely by reversed operation of neuronal glutamate transporters, and that it plays a key role in generating the anoxic depolarization that abolishes information processing in the central nervous system a few minutes after the start of ischaemia. A mathematical model incorporating K+ channels, reversible uptake carriers and NMDA (N-methyl-D-aspartate) receptor channels reproduces the main features of the response to ischaemia. Thus, transporter-mediated glutamate homeostasis fails dramatically in ischaemia: instead of removing extracellular glutamate to protect neurons, transporters release glutamate, triggering neuronal death.
 
  • #8
Andy Resnick
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