I am currently finishing my Ph.D. and have some results that I cant get my head around.
An angiotensin II treated KO mouse shows decreased stiffness of mesenteric resistance arteries and subsequent lower blood pressure compared to an angiotensin II treated WT mouse.
However, the KO mice show a significant higher max contractility to phenylephrine than WT mice (no difference in EC50) - does this make sense?
Can it be, that because the mesenteric resistance arteries are more compliant, they are able to max contract more than the WT mice?
So, stiff arteries has a lower max response to phenylephrine because the vascular smooth muscle cells work against more stiffness and thus more force??
I cant find anything about this in the litterature.
Thank you,
Kimmie
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