Aubrey de Grey wrote:
> Since (if I understand it) Richard's model involves a potential difference
> between regions that are connected by a virtually perfect conductor (the
> cytosol), I have difficulty seeing how Guy can be wrong that the influx of
> cations at the plasma membrane raises the potential at the mitochondrial
> membrane. But the inference that the mitochondrial delta-psi oscillates
> by an amount similar to that at the plasma membrane may be wrong, if there
> is a very rapid compensatory response that imports cations into the matrix.
> I am currently rather enamoured of the ATP- (and also GTP-, GDP- and more)
> sensitive potassium channel, which has been strongly implicated in the
> homeostasis of mitochondrial volume (an important regulator of OXPHOS); it
> also seems to stabilise delta-p, by adjusting the contributions of delta-pH
> and delta-psi in response to changing cytosolic cation concentrations.
> Czyz et al. 1995, BBRC 210:98-104 has details. Might it be involved here?
>> Aubrey de Grey
The mitochondrial ATP sensitive K+ channel has intriguing to those in
cardiovascular research, because of its potential role in ischemic
preconditioning.
Ischemic preconditioning is a phenomenon whereby a short period of ischemia
protects tissue from injury from a much longer period of ischemia. KATP
channel
openers mimic preconditioning, but recently there is evidence that the
mitochondrial
KATP channel might be the target rather than the plasma membrane channel.
However,
it is really unclear how opening KATP channels could be protective. Would it
somehow preserve mitochondrial function? I don't know what mitochondrial K+
is, but K can not be in equilibrium -> with a -200mV potential, it would imply
a molar concentration of mitochondrial K. Opening KATP channels would seem
to cause a large K+ mitochondria influx. I wonder what effects this would
have.
