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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Androgens and Non-Genomic vascular responses in hypertension
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<blockquote data-quote="madman" data-source="post: 229739" data-attributes="member: 13851"><p><strong>Fig. 3. <u>The most recognized non-genomic mechanisms of vasorelaxing/ hypotensive action</u>. 1) Restriction of extracellular Ca2+ entry by androgens to block L-type voltage-operated Ca2+ channel (L-VOCCs). TES shares the same molecular target as the dihydropyridines (the α1C subunit of L-VOCCs). 2) Restriction of extracellular Ca2+ entry through blockage of the receptor-operated Ca2+ channels (ROCCs). Restricting extracellular Ca2+ entry and diminishing intracellular Ca2+ concentration in the vascular smooth muscle cell induce vasorelaxation and hypotensive response. 3) TES activates voltage-sensitive K+ channels (Kv) or large-conductance–Ca2+-activate K+ channels (KCa), increasing K+ efflux to induce VSM hyperpolarization and vasorelaxation. 4) A partial endothelium-dependent mechanism has been suggested, presumably involving endothelium-derived relaxing factors from endothelial cells, particularly nitric oxide (NO), which would seem to be responsible for the vasorelaxing effect of TES; however, controversy exists (see discussion in 2.3 section).</strong></p><p><strong>[ATTACH=full]24459[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 229739, member: 13851"] [B]Fig. 3. [U]The most recognized non-genomic mechanisms of vasorelaxing/ hypotensive action[/U]. 1) Restriction of extracellular Ca2+ entry by androgens to block L-type voltage-operated Ca2+ channel (L-VOCCs). TES shares the same molecular target as the dihydropyridines (the α1C subunit of L-VOCCs). 2) Restriction of extracellular Ca2+ entry through blockage of the receptor-operated Ca2+ channels (ROCCs). Restricting extracellular Ca2+ entry and diminishing intracellular Ca2+ concentration in the vascular smooth muscle cell induce vasorelaxation and hypotensive response. 3) TES activates voltage-sensitive K+ channels (Kv) or large-conductance–Ca2+-activate K+ channels (KCa), increasing K+ efflux to induce VSM hyperpolarization and vasorelaxation. 4) A partial endothelium-dependent mechanism has been suggested, presumably involving endothelium-derived relaxing factors from endothelial cells, particularly nitric oxide (NO), which would seem to be responsible for the vasorelaxing effect of TES; however, controversy exists (see discussion in 2.3 section). [ATTACH type="full"]24459[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Androgens and Non-Genomic vascular responses in hypertension
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