I am afraid it does not really answer my question directly. If you are saying that there is no difference in the way olmesartan activates the VDR as compared to vitamin 1,25 once docked in to the LBP, how can olmesartan activate the VDR in a more controllable manner? (Come to think of it, maybe you said in earlier posts that olmesartan activates many other receptors than the VDR in a more controllable manner? Then I am sorry for the confusion)
Inge
____________________ CFS/ME 125D64 25D12(dec 07) Ph1De06 daily lite exp NoIR use Ph2Mar07 ModPh2 Jun07 abx brkOct 07 r//t KFTs freq abx chg to control kidney IP Apr 08 phase 2 abx
Inge,
The FDA has a mantra "It's all a matter of Dose."
The agonist effect of Olmesartan occurs at higher doses, and the degree of effect can be adjusted by adjusting the dose.
Whereas with a drug which is too high an affinity, like Telmisartan as an antagonist, you cannot adjust the dose to modulate the degree of the effect.
So Olmesartan is able to displace 1,25-D, or capnine, from the VDR LBP in a controlled manner, dependent on Olmesartan dose (and the concentration of capnine or 1,25-D).
This is called "homologous displacement" in most pharmacology texts. It follows a characteristic S-shaped curve.
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