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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Vascular Pathways of Testosterone: Clinical Implications
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<blockquote data-quote="madman" data-source="post: 165909" data-attributes="member: 13851"><p>[ATTACH=full]8804[/ATTACH]</p><p><strong><span style="color: rgb(184, 49, 47)">Fig. 2 </span></strong> <strong>Schematic representation of the overlap vasodilator genomic and non-genomic mechanisms of androgens. </strong><span style="color: rgb(250, 197, 28)"><strong>The yellow numbers represent the genomic actions</strong></span> <span style="color: rgb(44, 130, 201)"><strong>and the blue numbers represent the non-genomic actions. </strong></span><span style="color: rgb(250, 197, 28)"><strong>(1) </strong></span><span style="color: rgb(0, 0, 0)"><strong>Androgens cross the plasma membrane and enter the cytoplasm,where it dissociates from chaperone proteins and bind to androgen receptors (AR). </strong></span><span style="color: rgb(250, 197, 28)"><strong>(2)</strong></span><strong><span style="color: rgb(0, 0, 0)"> Androgens increase the H2S production and leads to vasodilation via TRPV4 and BKCa. </span><span style="color: rgb(250, 197, 28)">(3)</span> <span style="color: rgb(0, 0, 0)">Androgens upregulate β1 subunit BKCa.</span> <span style="color: rgb(250, 197, 28)">(4)</span><span style="color: rgb(184, 49, 47)"> </span><span style="color: rgb(0, 0, 0)">Androgens downregulate L-type VOCC. </span><span style="color: rgb(44, 130, 201)">(5)</span><span style="color: rgb(0, 0, 0)"> Androgens activate the ZIP9 and lead to a cAMP increase.</span> <span style="color: rgb(44, 130, 201)">(6)</span> Through binding to GPRC6A (Giα-activation), androgens lead to a cAMP decrease and ERK pathway activation. These two mechanisms modulate intracellular Ca2+ levels and lead to vasodilation through mechanisms still unknown. <span style="color: rgb(44, 130, 201)">(7)</span> Through binding to Giα, androgens are thought to activate particulate guanil cyclase, by a mechanism that is not yet known. <span style="color: rgb(44, 130, 201)">(8)</span> Androgens are thought to activate protein receptors, leading to a cGMP increase by particulate guanil cyclase activation. This increase in cGMP levels leads to PKG activation. Through PKG activation, androgens activate <span style="color: rgb(44, 130, 201)">(9)</span> K v and <span style="color: rgb(44, 130, 201)">(10)</span> BKCa channels and inactivate</strong><span style="color: rgb(44, 130, 201)"> <strong>(11)</strong></span> <strong>L-type VOCC channels through mechanisms still unknown. </strong><span style="color: rgb(44, 130, 201)"><strong>(12)</strong></span> <strong>Via androgen receptors (AR), it is thought that these sex hormones inhibit particulate guanil cyclase.</strong></p></blockquote><p></p>
[QUOTE="madman, post: 165909, member: 13851"] [ATTACH=full]8804[/ATTACH] [B][COLOR=rgb(184, 49, 47)]Fig. 2 [/COLOR][/B] [B]Schematic representation of the overlap vasodilator genomic and non-genomic mechanisms of androgens. [/B][COLOR=rgb(250, 197, 28)][B]The yellow numbers represent the genomic actions[/B][/COLOR] [COLOR=rgb(44, 130, 201)][B]and the blue numbers represent the non-genomic actions. [/B][/COLOR][COLOR=rgb(250, 197, 28)][B](1) [/B][/COLOR][COLOR=rgb(0, 0, 0)][B]Androgens cross the plasma membrane and enter the cytoplasm,where it dissociates from chaperone proteins and bind to androgen receptors (AR). [/B][/COLOR][COLOR=rgb(250, 197, 28)][B](2)[/B][/COLOR][B][COLOR=rgb(0, 0, 0)] Androgens increase the H2S production and leads to vasodilation via TRPV4 and BKCa. [/COLOR][COLOR=rgb(250, 197, 28)](3)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR][COLOR=rgb(0, 0, 0)]Androgens upregulate β1 subunit BKCa.[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR][COLOR=rgb(250, 197, 28)](4)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR][COLOR=rgb(0, 0, 0)]Androgens downregulate L-type VOCC. [/COLOR][COLOR=rgb(44, 130, 201)](5)[/COLOR][COLOR=rgb(0, 0, 0)] Androgens activate the ZIP9 and lead to a cAMP increase.[/COLOR] [COLOR=rgb(44, 130, 201)](6)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR]Through binding to GPRC6A (Giα-activation), androgens lead to a cAMP decrease and ERK pathway activation. These two mechanisms modulate intracellular Ca2+ levels and lead to vasodilation through mechanisms still unknown. [COLOR=rgb(44, 130, 201)](7)[/COLOR] Through binding to Giα, androgens are thought to activate particulate guanil cyclase, by a mechanism that is not yet known. [COLOR=rgb(44, 130, 201)](8)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR]Androgens are thought to activate protein receptors, leading to a cGMP increase by particulate guanil cyclase activation. This increase in cGMP levels leads to PKG activation. Through PKG activation, androgens activate [COLOR=rgb(44, 130, 201)](9)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR]K v and[COLOR=rgb(184, 49, 47)] [/COLOR][COLOR=rgb(44, 130, 201)](10)[/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR]BKCa channels and inactivate[/B][COLOR=rgb(44, 130, 201)] [B](11)[/B][/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR][B]L-type VOCC channels through mechanisms still unknown. [/B][COLOR=rgb(44, 130, 201)][B](12)[/B][/COLOR][COLOR=rgb(184, 49, 47)] [/COLOR][B]Via androgen receptors (AR), it is thought that these sex hormones inhibit particulate guanil cyclase.[/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Vascular Pathways of Testosterone: Clinical Implications
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