Title : NHE inhibition does not improve Na(+) or Ca(2+) overload during reperfusion: using modeling to illuminate the mechanisms underlying a therapeutic failure.

Pub. Date : 2011 Oct

PMID : 22028644






3 Functional Relationships(s)
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1 Events in the development of reperfusion injury begin with the restoration of a proton gradient upon reperfusion, which then allows the sodium-proton exchanger (NHE) to increase flux, removing protons from the intracellular space while importing sodium. Sodium solute carrier family 9 member C1 Homo sapiens
2 In our simulations, when NHE inhibition is applied at the onset of reperfusion, increasing the degree of inhibition increases the peak sodium and calcium concentrations, as well as reducing intracellular pH recovery. Sodium solute carrier family 9 member C1 Homo sapiens
3 While NHE inhibition does indeed reduce sodium influx through that exchanger, the resulting prolongation of intracellular acidosis paradoxically increases sodium overload, largely mediated by impaired NaK function. Sodium solute carrier family 9 member C1 Homo sapiens