According to Goljan- Hypoxemia results in respiratory alkalosis. And alkalosis activates PFK in order to compensate shifting OBC to the right.
But then I read in BRS that PFK is activated as a result of hypoxic cell injury.
So my question is, are these two completely different mechanisms?
Logically, ATP depletion would activate PFK, driving the metabolism into an anaerobic glycolisis state. But how does alkalosis activate PFK?
But then I read in BRS that PFK is activated as a result of hypoxic cell injury.
So my question is, are these two completely different mechanisms?
Logically, ATP depletion would activate PFK, driving the metabolism into an anaerobic glycolisis state. But how does alkalosis activate PFK?