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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: 211228" data-attributes="member: 13851"><p><strong>Fig. 7. <u>Smooth muscle contraction pathways</u>. Upon stimulation of adrenergic nerves (lightning bolt), noradrenaline (NA) is released and binds to the α1-adrenoreceptor (α1). Endothelin-1 (ET-1), angiotensin-II (Ang-II), and the prostanoid thromboxane A2 (TXA2) released from the endothelial cell bind to their receptors ETA, AT1, and TP, respectively, on the smooth muscle cell. Association of these ligands with their receptors leads to activation of phospholipase C (PLC), which then produces inositol triphosphate 3 (IP3) and diacylglycerol (DAG). IP3 is associated with the IP3 receptor (IP3R) on the sarcoplasmic reticulum (SR), which acts as a channel to release Ca2+ from the SR. The activated IP3Rs couple with membrane-bound transient receptor potential canonical 3 (TRPC3) channels, leading to an influx of extracellular Ca2+. Increased cytosolic Ca2+ in the smooth muscle cell causes depolarization (DP), activating Ca2+ channels in the smooth muscle cell membrane which leads to a further influx of Ca2+. DAG leads to activation of protein kinase C (PKC), which activates CPI-17 by phosphorylation. This then inhibits MLCP. Association of NA, ETA, Ang-II, and TXA2 with their receptors may also drive the RhoA/Rho-kinase pathway to inhibit MLCP. Thus, these signaling factors drive smooth muscle cell contraction by increasing cytosolic Ca2+ and increasing Ca2+ sensitivity. MLCP is the same as shown in Figure 3.</strong></p><p><strong>[ATTACH=full]17382[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 211228, member: 13851"] [B]Fig. 7. [U]Smooth muscle contraction pathways[/U]. Upon stimulation of adrenergic nerves (lightning bolt), noradrenaline (NA) is released and binds to the α1-adrenoreceptor (α1). Endothelin-1 (ET-1), angiotensin-II (Ang-II), and the prostanoid thromboxane A2 (TXA2) released from the endothelial cell bind to their receptors ETA, AT1, and TP, respectively, on the smooth muscle cell. Association of these ligands with their receptors leads to activation of phospholipase C (PLC), which then produces inositol triphosphate 3 (IP3) and diacylglycerol (DAG). IP3 is associated with the IP3 receptor (IP3R) on the sarcoplasmic reticulum (SR), which acts as a channel to release Ca2+ from the SR. The activated IP3Rs couple with membrane-bound transient receptor potential canonical 3 (TRPC3) channels, leading to an influx of extracellular Ca2+. Increased cytosolic Ca2+ in the smooth muscle cell causes depolarization (DP), activating Ca2+ channels in the smooth muscle cell membrane which leads to a further influx of Ca2+. DAG leads to activation of protein kinase C (PKC), which activates CPI-17 by phosphorylation. This then inhibits MLCP. Association of NA, ETA, Ang-II, and TXA2 with their receptors may also drive the RhoA/Rho-kinase pathway to inhibit MLCP. Thus, these signaling factors drive smooth muscle cell contraction by increasing cytosolic Ca2+ and increasing Ca2+ sensitivity. MLCP is the same as shown in Figure 3. [ATTACH type="full"]17382[/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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