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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Hypertension and erectile dysfunction: breaking down the challenges
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<blockquote data-quote="madman" data-source="post: 186292" data-attributes="member: 13851"><p>[ATTACH=full]10654[/ATTACH]</p><p><strong><span style="color: rgb(0, 0, 0)">Figure 2. </span><span style="color: rgb(184, 49, 47)">Overview of the major pathways shared by hypertension and ED.</span> During hypertension, there is an increase in the release of vasoconstrictor peptides <span style="color: rgb(184, 49, 47)">(e.g., AngII, ET-1, aldosterone)</span>, which via specific receptors trigger NADPH oxidase-induced ROS. In fact, ROS is a hub mechanism that crosstalks with many pathways that are important for the maintenance of vascular and erectile function. An increase in the release of ROS activates the RhoA/Rho-kinase pathway, associates with premature vascular aging, stimulates the transcriptional factors Nrf2 and NF- кB, and impairs NO availability. Simultaneously, activation of TLR4 also induces the stimulation of NF- кB, which not only affects ROS but also induces the release of pro-inflammatory mediators. Additionally, while ROS stimulates Nrf2, the activation of Nrf2 per se leads to the expression of antioxidant genes, which aims at inhibiting the effects of ROS. Nfr2 is also stimulated by the gaseous transmitter H2S, which has many compensatory functions, including the inhibition of the PDE5 enzyme. In hypertensive conditions, it also appears that the Ang1-7/Mas receptor axis, which counterbalances the effects of the AngII/AT1r axis, elicits an inefficient response.</strong></p></blockquote><p></p>
[QUOTE="madman, post: 186292, member: 13851"] [ATTACH type="full"]10654[/ATTACH] [B][COLOR=rgb(0, 0, 0)]Figure 2. [/COLOR][COLOR=rgb(184, 49, 47)]Overview of the major pathways shared by hypertension and ED.[/COLOR] During hypertension, there is an increase in the release of vasoconstrictor peptides [COLOR=rgb(184, 49, 47)](e.g., AngII, ET-1, aldosterone)[/COLOR], which via specific receptors trigger NADPH oxidase-induced ROS. In fact, ROS is a hub mechanism that crosstalks with many pathways that are important for the maintenance of vascular and erectile function. An increase in the release of ROS activates the RhoA/Rho-kinase pathway, associates with premature vascular aging, stimulates the transcriptional factors Nrf2 and NF- кB, and impairs NO availability. Simultaneously, activation of TLR4 also induces the stimulation of NF- кB, which not only affects ROS but also induces the release of pro-inflammatory mediators. Additionally, while ROS stimulates Nrf2, the activation of Nrf2 per se leads to the expression of antioxidant genes, which aims at inhibiting the effects of ROS. Nfr2 is also stimulated by the gaseous transmitter H2S, which has many compensatory functions, including the inhibition of the PDE5 enzyme. In hypertensive conditions, it also appears that the Ang1-7/Mas receptor axis, which counterbalances the effects of the AngII/AT1r axis, elicits an inefficient response.[/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Hypertension and erectile dysfunction: breaking down the challenges
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