Hypertension I: Structure of Small Arteries in Hypertension

Re: To Dr. Lehoux

Stephanie Lehoux

On Mon Dec 14, Jos P.M. Wesselman wrote
>Dr. Lehoux,
>   I really like your paper about the differences in signal transduction with static and pulsatile stretch. I have a question about the experiments where you observe an increased MAPK activity at 150 mmHg, as compared to control pressure. You found that herbimycin A reduced this pressure-induced increase. Did you also test the effect of herbimycin A at control pressure?
Thank you for your question Dr Wesselman

We did not in fact test herbimycin A against baseline MAP kinase activity at control pressures. However, since this drug blocked steady stretch-induced MAP kinase activation but not pulsatile stretch- induced activation, I suspect that the effects we see with herbimycin A are rather specific for steady stretch. Furthermore, they coincide with conditions where FAK is also activated (compared to vessels at control pressure), which points to a possible transduction pathway of steady stretch involving interaction of Src-family tyrosine kinases with FAK and subsequent downstream activation of MAP kinase.

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