Page 2 of 3: mechanism of action of estrogen?

docsa · Credits: 9033 My Scrapbook

sorry docs wanna correct u
KDT 5ed p-214 clearly says estrogen acts at CYTOPLASMIC RECEPTORS

only thyroid hormones act at nuclear receptors

AHMADDD · Credits: 5921 My Scrapbook My Reading List 1 Books

via cytoplasmic receptors

sea_corel · Credits: 11951 My Scrapbook My Reading List 7 Books

Multiple mechanisms are involved in the actions of estrogen in different tissues.The effects of estrogen are mediated by estrogen receptors, estrogen receptor-α (ER-α) and estrogen receptor-β (ER-β ). Estrogen receptors are expressed not only in reproductive tissues but they are also found in myocardial, endothelial and vascular smooth muscle cells, liver, breast, brain and bone. These receptors are targets for both endogenous and exogenous estrogens and pharmacological estrogen agonists, but they can also be activated by growth factors. Similar mechanisms for estrogen action have been described in different cells, the action can however be mediated by different signaling pathways. The classic signaling pathway for estrogen action is the ligand-dependent receptor activation pathway in which activated estrogen receptors are transcription factors that alter gene expression and increase protein synthesis). The ligand-independent activation of estrogen receptors for example by growth factors also results in nuclear actions. In addition to these transcriptional mechanisms the non-nuclear estrogen-signaling pathway through cell-membrane estrogen receptors is suggested to be involved in rapid responses to estrogen.

Molecular actions of estrogens are determined by the structure of the hormone, the subtype or isoform of the estrogen receptor involved, the target gene promotor, and the balance of coactivators and corepressors that modulate the transcriptional activity

jayanta · Credits: 34192 My Scrapbook My Reading List 45 Books

it is definitely on the nucleus.

cma · Credits: 1011 My Scrapbook My Reading List 3 Books

but in pharma books it is mentioned that thyroid hormes bind nuclear receptors and steroid hormones bind receptors in cytoplasm and then enter nucleus for transcription

ujwals · Credits: 4860 My Scrapbook

cytoplasm

ujwals · Credits: 4860 My Scrapbook

the hormone gene superfamily is divided into three subfamilies-

TYPE I includes the classical steroid receptors which include-

glucocorticoid receptors(including cortisol)
androgen receptors
mineralcorticoid receptors(including aldosterone)
progesterone receptors

TYPE II includes the thyroid related receptors('related' refers to retinoid receptors apart frm the thyroid receptors) and dihydroxy vitamin D3 receptors.

TYPE III includes the estrogen receptors & orphan receptors(orphan receptors r those for which no binding ligands hav been described,till date!) icon_eek.gif

out of these TYPE I & III hav cytoplasmic receptors.
while TYPE II bind directly to the nuclear receptors.

(pasted from a another post)

jayanta · Credits: 34192 My Scrapbook My Reading List 45 Books

IT'S NUCLEUS.
REGARDS.

Vagus · Credits: 234 My Scrapbook

can you tell me what is osler's sign

quincy · Credits: 3567 My Scrapbook

Osler's sign, the ability to palpate the stiff, thickened radial artery when the sphygmomanometric cuff is inflated to suprasystolic BP,

Pseudohypertension refers to falsely elevated systolic BP readings in elderly patients with very stiff arteries. Pseudohypertension occurs because the BP cuff cannot completely occlude the artery. Osler's sign, the ability to palpate the stiff, thickened radial artery when the sphygmomanometric cuff is inflated to suprasystolic BP, was once thought to suggest pseudohypertension, but more recent studies suggest that Osler's sign is an unreliable marker for this condition.
Alternative ways to distinguish true systolic hypertension from pseudohypertension include arm x-rays to document extensive vascular calcification and Doppler flow studies, but neither is routine practice. More commonly, pseudohypertension is diagnosed when elderly patients do not respond to treatment, have markedly elevated systolic BP without signs of end-organ damage, or develop signs of hypotension (eg, fatigue, orthostasis) despite persistently elevated BP measurements.

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