riversinger
Frequent Contributor (1K+ posts)
Member # 4851
posted
You have to read the Marshall Protocol info on angiotensin and 1,25-D to understand how these articles might relate. It seems to me there is a complex feedback loop between all of these hormones. If you search pubmed, you will find more.
Insulin and progesterone production are also involved in some of this complex interplay.
Downregulation of vascular angiotensin II type 1 receptor by thyroid hormone.
Fukuyama K, Ichiki T, Takeda K, Tokunou T, Iino N, Masuda S, Ishibashi M, Egashira K, Shimokawa H, Hirano K, Kanaide H, Take****a A.
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, 812-8582 Fukuoka, Japan.
Thyroid hormone has a broad effect on cardiovascular system. 3,3',5-triiodo-l-thyronine (T3), a biologically active form of thyroid hormone, increases cardiac contractility. T3 causes arterial relaxation and reduction of systemic vascular resistance, resulting in an increase in cardiac output. However, the molecular mechanisms of vascular relaxation by T3 are incompletely characterized. We studied the effect of T3 on the angiotensin (Ang) II type 1 receptor (AT1R) expression in vascular smooth muscle cells. T3 dose-dependently decreased expression levels of AT1R mRNA, with a peak at 6 hours of stimulation. Binding assay using [125I]Sar1-Ile8-Ang II revealed that AT1R number was decreased by stimulation with T3 without changing the affinity to Ang II. T3 reduced calcium response of vascular smooth muscle cells to Ang II by 26%. AT1R promoter activity measured by luciferase assay was reduced by 50% after 9 hours of T3 administration. mRNA stability was also decreased by T3. Real-time quantitative reverse transcription-polymerase chain reaction and Western blot analysis revealed that AT1R mRNA and protein were downregulated in the aorta of T3-treated rats. These results suggest that T3 downregulates AT1R expression both at transcriptional and posttranscriptional levels, and attenuates biological function of Ang II. Our results suggest that downregulation of AT1R gene expression may play an important role for T3-induced vascular relaxation.
PMID: 12623965 [PubMed - indexed for MEDLINE]
[This message has been edited by riversinger (edited 31 August 2004).]
riversinger
Frequent Contributor (1K+ posts)
Member # 4851
posted
Characterization of a 1,25-dihydroxy-vitamin D3 receptor in FRTL-5 cells. Evidence for an inhibitory effect of 1,25-dihydroxy-vitamin D3 on thyrotropin-induced iodide uptake.
Lamberg-Allardt C, Valtonen E, Polojarvi M, Stewen P.
Endocrine Research Laboratory, University of Helsinki, Finland.
When FRTL-5 cell cytosol was incubated with increasing amounts of [3H]1,25-dihydroxy-vitamin D3 [( 3H]1,25-(OH)2D3), saturation of specific hormone binding occurred. Scatchard analysis of specific binding of [3H]1,25-(OH)2D3 to the macromolecule yielded an apparent Kd value of 0.41 +/- 0.08 X 10(-10) M and a single maximum binding capacity of 42.8 +/- 8.8 fmol/mg protein. Sucrose gradient analysis revealed substantial [3H]1,25-(OH)2D3 association with a macromolecule sedimentating slightly faster than ovalbumin (3.7 S). [3H]1,25-(OH)2D3 was completely displaced by excess 1,25-(OH)2D3. The 1,25-(OH)2D3-receptor complex bound to DNA cellulose columns in low salt buffer, and eluted as a single peak at 0.15-0.20 M KCl. Thus, we have shown for the first time the existence of a functional 1,25-(OH)2D3 receptor in thyroid follicular cells. Furthermore, 1,25-(OH)2D3 inhibited the thyrotropin (TSH)-stimulated iodide uptake in a dose-dependent manner, indicating that 1,25-(OH)2D3 has an effect on the physiological function of rat thyroid follicular cells in culture.
riversinger
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Member # 4851
posted
Pituitary 1,25-dihydroxyvitamin D3 receptors in hyperthyroid- and hypothyroid-rats.
Kashio Y, Iwasaki J, Chihara K, Kaji H, Kita T, Okimura Y, Fujita T.
The binding of 1 alpha,25-dihydroxy (26,27-methyl-[3H]) cholecalciferol ([3H]1,25-(OH)2D3) to its receptor in cytosol of the anterior pituitary cells was examined in hyperthyroid- and hypothyroid rats, as well as in normal rats. The binding capacity increased by 41% in L-Thyroxine-treated hyperthyroid rats and decreased by 49% in propylthiouracil-ingested hypothyroid rats as compared with normal control rats, whereas the affinity of the receptor for [3H]-1,25(OH)2D3 showed no difference among these 3 animal groups. These findings indicate that the number of 1,25(OH)2D3 receptors in the pituitary may be regulated by thyroid hormone, and further suggest that 1,25-(OH)2D3 may play some role in regulating functions of the anterior pituitary.
minoucat
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Member # 5175
posted
Curioser and curioser. Very interesting in light of the thyroid storms some MP users experience. I have almost no inflammation at all now, and my thyroid function appears to be completely normal again -- it was on the low side for a while. Also, my hypoglycemia is completely gone. It would have been interesting to have done the 1,25D measurements when I was sickest and most inflamed. (I've never done the MP, but I'm pleased to keep hearing about it.)
[This message has been edited by minoucat (edited 31 August 2004).]
riversinger
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Member # 4851
posted
Yes, it's pretty interesting. Like I said, I found abstracts relating angiotensin to insulin and insulin resistence, which would of course have an impact on hypoglycemia.
I'm thinking there is, as usual, more than one way to skin a cat. Oops, not you, minou! This illness. High dose, low dose, MP, IV, pulsed may all end up having their uses.
You have discovered a wealth of information. That's why I always love reading you : )
I'm hitting print so that I can carry this with me on vacation. (It's our first real, out of the state vacation in a couple of years. Yay! I'll try and post a MP update when I get back.)
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Oops, not you, minou! This illness. High dose, low dose, MP, IV, pulsed may all end up having their uses.
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