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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
ED in Men on the Rise: Is There a Link with Endocrine Disrupting Chemicals?
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<blockquote data-quote="madman" data-source="post: 211227" data-attributes="member: 13851"><p><strong>Fig. 6. <u>NO sources and other factors which drive smooth muscle relaxation</u>. The NO-cGMP pathway reduces cytosolic Ca2+ and inhibits the RhoA/Rho-kinase pathway as depicted in Figure 4. When the NANC nerves are stimulated (lightning bolt), Ca2+ binds to calmodulin to form the calmodulin-Ca2+ (Cam-Ca2+) complex. This subsequently binds to and activates neuronal NOS (nNOS), driving NO production. Also, stimulation of NANC nerves drives the production of cAMP in these cells. This activates protein kinase A (PKA) which in turn activates nNOS by phosphorylation (P). The initial production of NO by the NANC nerves leads to smooth muscle cell (SMC) relaxation, in turn leading to shear stress on the endothelial cells. This triggers the PI3K/Akt pathway, which then activates eNOS by phosphorylation. Acetylcholine released from cholinergic nerves binds to the muscarinic acetylcholine receptor (mAChR), which increases Ca2+ in the endothelial cell. This leads to the formation of Cam-Ca2+, which binds to and activates eNOS. Endogenous estrogen signaling also activates eNOS by stimulating the PI3K/Akt pathway and upregulating the expression of eNOS (see Fig. 5). In addition to the NO-cGMP pathway, vasoactive intestinal peptide (VIP) in the NANC nerves may bind to its receptor (VIP-R) on the smooth muscle cell to stimulate soluble adenylyl cyclase (sAC). This leads to the production of cAMP in the smooth muscle cell, activating PKA to reduce cytosolic Ca2+ concentration. cAMP may also mediate smooth muscle cell relaxation via activation of PKG. The prostanoids prostaglandin E2 (PGE2) and prostacyclin (PGI2) can also drive cAMP production via association with the EP and IP receptors on the smooth muscle cell, respectively. NANC is the same as shown in Figure 2sGC, PKG and NO are the same as shown in Figure 4. PI3K/Akt and eNOS are the same as shown in Figure 5.</strong></p><p><strong>[ATTACH=full]17381[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 211227, member: 13851"] [B]Fig. 6. [U]NO sources and other factors which drive smooth muscle relaxation[/U]. The NO-cGMP pathway reduces cytosolic Ca2+ and inhibits the RhoA/Rho-kinase pathway as depicted in Figure 4. When the NANC nerves are stimulated (lightning bolt), Ca2+ binds to calmodulin to form the calmodulin-Ca2+ (Cam-Ca2+) complex. This subsequently binds to and activates neuronal NOS (nNOS), driving NO production. Also, stimulation of NANC nerves drives the production of cAMP in these cells. This activates protein kinase A (PKA) which in turn activates nNOS by phosphorylation (P). The initial production of NO by the NANC nerves leads to smooth muscle cell (SMC) relaxation, in turn leading to shear stress on the endothelial cells. This triggers the PI3K/Akt pathway, which then activates eNOS by phosphorylation. Acetylcholine released from cholinergic nerves binds to the muscarinic acetylcholine receptor (mAChR), which increases Ca2+ in the endothelial cell. This leads to the formation of Cam-Ca2+, which binds to and activates eNOS. Endogenous estrogen signaling also activates eNOS by stimulating the PI3K/Akt pathway and upregulating the expression of eNOS (see Fig. 5). In addition to the NO-cGMP pathway, vasoactive intestinal peptide (VIP) in the NANC nerves may bind to its receptor (VIP-R) on the smooth muscle cell to stimulate soluble adenylyl cyclase (sAC). This leads to the production of cAMP in the smooth muscle cell, activating PKA to reduce cytosolic Ca2+ concentration. cAMP may also mediate smooth muscle cell relaxation via activation of PKG. The prostanoids prostaglandin E2 (PGE2) and prostacyclin (PGI2) can also drive cAMP production via association with the EP and IP receptors on the smooth muscle cell, respectively. NANC is the same as shown in Figure 2sGC, PKG and NO are the same as shown in Figure 4. PI3K/Akt and eNOS are the same as shown in Figure 5. [ATTACH type="full"]17381[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
ED in Men on the Rise: Is There a Link with Endocrine Disrupting Chemicals?
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