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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Penis smaller after TRT
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<blockquote data-quote="madman" data-source="post: 204454" data-attributes="member: 13851"><p>Underlying vascular health is critical.</p><p></p><p>Blood flow to the penis will have a big impact on the size when flaccid and on the strength/size when erect.</p><p></p><p></p><p><em><strong>Erectile function is controlled by complex mechanisms, including the vascular and nervous systems. <u>One of the most important materials is nitric oxide (NO)</u>.</strong></em> After NO is releasing in the penis, the corporal smooth muscle relaxes. However, when NO production is decreased, the erectile function weakened, resulting in ED. <strong><em>The relaxant system is also important for erectile function. The relaxant system is controlled by both the endothelial and the nervous systems. </em></strong>When the upper stream of the smooth muscle relaxant system is weakened, ED is caused; therefore, many studies have focused on smooth muscle relaxation. <strong><em><u>In contrast, corporal smooth muscle contraction is controlled by constrictors, such as noradrenaline in the flaccid state</u>. </em></strong>However, if the contraction is upregulated in some situations, ED would be caused.</p><p></p><p><strong><em>Interestingly, some studies have indicated that smooth muscle relaxation and contraction balance is disturbed by abnormal activation of contractile signaling pathway such as the adrenergic regulation.</em></strong> In some syndromes causing ED, such as diabetes mellitus or metabolic syndrome, the contraction is enhanced. One of the important contractile signaling pathways is the RhoA/Rho-kinase signaling pathway. The enhancement is known to occur in aged individuals. The inhibition of the RhoA/Rho-kinase signaling pathway by Y-27632 has been shown to improve ED in aged animal models.<strong><em> Interestingly, the contractility of smooth muscle in the corpus cavernosum is regulated by sexual hormones and may play a significant role in erectile function.</em></strong></p><p></p><p></p><p><em><strong>*In the flaccid state of the penis, <u>which is dominated by the adrenergic tone of the smooth muscles under the influence of the sympathetic part of the autonomic nervous system</u>, the arterial flow is low, based on the constricted arterioles and the contracted cavernosal smooth muscles</strong></em></p><p></p><p></p><p></p><p></p><p><strong><em>Overall, efficacy for the different PDE5 inhibitors rates is 60–70% with on-demand treatment regimens (Albertsen et al., 2010). Of the patients that initially do not respond to PDE5 inhibitors, between 30 and 50% may be converted to responders by counseling the patient and his partner. Some patients who fail to achieve an erection when taking PDE5 inhibitors on-demand benefit from a daily dosing regimen. Furthermore, in the male suffering from ED in the context of late-onset hypogonadism, the addition of testosterone supplementation might enhance PDE5 inhibitor therapy.</em></strong></p><p><strong><em></em></strong></p><p><strong><em>As the efficacy of PDE5 inhibitors depends on <u>the integrity of the NO pathway in producing cGMP</u>, it is evident that patients in whom this pathway is disturbed or defective will benefit far less than the general population from PDE5 inhibitors.</em></strong></p><p><strong><em></em></strong></p><p><strong><em>*Disease states that <u>diminish NO availability</u> include denervation of the erectile tissue following radical prostatectomy; severe diabetes with neuropathy and <u>endothelial dysfunction</u>; metabolic syndrome; and down-regulation of NOS expression as may be seen in atherosclerosis, aging, and hypogonadism.</em></strong></p><p><strong><em></em></strong></p><p><strong><em></em></strong></p><p><strong><em>An unimpaired neuronal innervation of the erectile tissue as well as intact cavernous structures, <u>providing for the production of sufficient amounts of NO from (vascular) endothelial or neuronal sources are pivotal for the pharmacological action of PDE5 inhibitors</u> </em></strong></p></blockquote><p></p>
[QUOTE="madman, post: 204454, member: 13851"] Underlying vascular health is critical. Blood flow to the penis will have a big impact on the size when flaccid and on the strength/size when erect. [I][B]Erectile function is controlled by complex mechanisms, including the vascular and nervous systems. [U]One of the most important materials is nitric oxide (NO)[/U].[/B][/I] After NO is releasing in the penis, the corporal smooth muscle relaxes. However, when NO production is decreased, the erectile function weakened, resulting in ED. [B][I]The relaxant system is also important for erectile function. The relaxant system is controlled by both the endothelial and the nervous systems. [/I][/B]When the upper stream of the smooth muscle relaxant system is weakened, ED is caused; therefore, many studies have focused on smooth muscle relaxation. [B][I][U]In contrast, corporal smooth muscle contraction is controlled by constrictors, such as noradrenaline in the flaccid state[/U]. [/I][/B]However, if the contraction is upregulated in some situations, ED would be caused. [B][I]Interestingly, some studies have indicated that smooth muscle relaxation and contraction balance is disturbed by abnormal activation of contractile signaling pathway such as the adrenergic regulation.[/I][/B] In some syndromes causing ED, such as diabetes mellitus or metabolic syndrome, the contraction is enhanced. One of the important contractile signaling pathways is the RhoA/Rho-kinase signaling pathway. The enhancement is known to occur in aged individuals. The inhibition of the RhoA/Rho-kinase signaling pathway by Y-27632 has been shown to improve ED in aged animal models.[B][I] Interestingly, the contractility of smooth muscle in the corpus cavernosum is regulated by sexual hormones and may play a significant role in erectile function.[/I][/B] [I][B]*In the flaccid state of the penis, [U]which is dominated by the adrenergic tone of the smooth muscles under the influence of the sympathetic part of the autonomic nervous system[/U], the arterial flow is low, based on the constricted arterioles and the contracted cavernosal smooth muscles[/B][/I] [B][I]Overall, efficacy for the different PDE5 inhibitors rates is 60–70% with on-demand treatment regimens (Albertsen et al., 2010). Of the patients that initially do not respond to PDE5 inhibitors, between 30 and 50% may be converted to responders by counseling the patient and his partner. Some patients who fail to achieve an erection when taking PDE5 inhibitors on-demand benefit from a daily dosing regimen. Furthermore, in the male suffering from ED in the context of late-onset hypogonadism, the addition of testosterone supplementation might enhance PDE5 inhibitor therapy. As the efficacy of PDE5 inhibitors depends on [U]the integrity of the NO pathway in producing cGMP[/U], it is evident that patients in whom this pathway is disturbed or defective will benefit far less than the general population from PDE5 inhibitors. *Disease states that [U]diminish NO availability[/U] include denervation of the erectile tissue following radical prostatectomy; severe diabetes with neuropathy and [U]endothelial dysfunction[/U]; metabolic syndrome; and down-regulation of NOS expression as may be seen in atherosclerosis, aging, and hypogonadism. An unimpaired neuronal innervation of the erectile tissue as well as intact cavernous structures, [U]providing for the production of sufficient amounts of NO from (vascular) endothelial or neuronal sources are pivotal for the pharmacological action of PDE5 inhibitors[/U] [/I][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
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Penis smaller after TRT
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