Thyroid Hormone Stimulates Nitric Oxide Production

Terma

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Hmm, interesting, I never connected that directly, but since thyroid is well known to activate PI3K/Akt, and in endo cells Akt will increase eNOS, I guess it follows. But in that sense any PI3K/Akt activator could increase eNOS in endo cells at the high enough dose and context. I suppose he might interpret it as a metabolic "brake", though if iNOS gets increased then it seems more like an "overload". [whereas the mainstream would say the eNOS is normal and iNOS is the brake running into overload]

Something to keep in mind (cited by yours): Rapid nongenomic actions of thyroid hormone
Although the concentrations of T3 that lead to TRE-dependent responses normally occur in the picomolar range, we found that the minimum concentrations of T3, which activate Akt and eNOS, are somewhat higher, within the dissociation constant for TR (i.e., 0.1–1 nM) (22). Indeed, in euthyroid human volunteers, injection of 100 μg of T3 increases free T3 in the serum to levels >62 pM and is required to rapidly decrease BP and systemic vascular resistance (30). These findings indicate that there are pharmacological effects of thyroid hormone on the cardiovascular system, which occur at concentrations well above what is required to initiate TRE-dependent responses. It remains to be determined, however, why higher concentrations of T3 are required for Akt and eNOS activation compared with that of TRE-dependent responses.
 
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ddjd

ddjd

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@dookie @Tarmander @Vida @RKIII @Abc123

Hi guys, thought i'd link you into this thread as we've previously discussed estrogenic symptoms after taking T3.

This study i posted above proves that T3 increases nitric oxide. And as peat talks about and as ive experienced, nitric oxide and estrogen are very closely related.

what's more interesting is that they say:

"The increase of NO production induced by T3 was completely abolished in cells pretreated with iNOS inhibitor (1400 W—100 µM) or with nNOS inhibitor (AAAN—10 µM). T3-induced NO production was completely abolished in cells pretreated with 1400 W plus AAAN, suggesting that the eNOS is not involved in this process (Figure 7C)."


Basically, my theory is taking a supplement that blocks nNOS and iNOS could very likely stop our estrogenic reaction to T3.

Things that block nNOS and iNOS are :

- methylene blue
- zinc
- agmatine
- minocycline


Has anyone ever tried taking T3 after methylene blue and noticed the same estrogenic reaction?
 

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