R Loch Macdonald
I was interested to read your work on MAPK and contraction. We have begun similar experiments using pure hemoglobin as the contractant. I note that you observed effects at 30 uM and above. The question arises as to whether you have carried out control measurements of the concentration of PD98? required to inhibit contraction to an agonist that is known to act via MAPK eg. thrombin and that that concentration does not affect contraction to eg. KCl. Second, what compound in the hemolysate does this? We previously found some of the effect of acute hemolysate is due to ATP but why, for example, would hemoglobin do this? IS it a direct or indirect effect?
Tue Dec 8