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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Anatomy, Pathophysiology, Molecular Mechanisms, and Clinical Management of ED in Patients Affected by CAD
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<blockquote data-quote="madman" data-source="post: 200132" data-attributes="member: 13851"><p><strong>Figure 1. Pathways of penile erection: Dilation of cavernosal arteries and smooth muscle cells (SMCs) of cavernosal spaces is mediated by the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway. NO is derived from nonadrenergic, noncholinergic nerves (nNOS, NOS type I), and the endothelium (eNOS or NOS type III) of cavernosal sinuses (both calcium2+/calmodulin-dependent isoforms). NO crosses plasma membranes to enter vascular smooth muscle cells (VSMCs) and promotes the synthesis and accumulation of cGMP, which induces a cascade reaction, leading to smooth muscle relaxation by reducing intracellular calcium levels. NNOS = neuronal nitric oxide. ENOS = endothelial nitric oxide. See the text for details. A physiological penile erection requires normal vascular, neurological, and tissue responses. Penile erection is initiated after the central stimulus and integration of tactile, visual, olfactory, and imaginative triggers. Different observations demonstrate a network of afferent fibers from the genitals, spinal interneurons, and sympathetic, parasympathetic, and somatic nuclei, receiving stimulus from the periphery at the spinal cord level triggering reflexive erections. This network seems to receive also supraspinal information. At the level of the central nervous tissue, afferent data is processed in the forebrain and hypothalamus. In this latter area, the medial preoptic center, paraventricular nucleus, and anterior hypothalamic regions regulate erections and modulate autonomic events associated with sexual response. Different efferent pathways are present between the hypothalamus and sacral autonomic centers represented by the thoracolumbar and sacral autonomic nuclei. The erectile activity is finally coordinated by autonomic fibers network to the penis and somatic fibers pathways to the perineal striated muscles, responsible, in turn, for penis sensation. The cavernosal nerves originate from the autonomic system and are made of both sympathetic and parasympathetic fibers. These fibers travel along the prostate and enter the corpus spongiosum and the corpora cavernosa to regulate the blood flow during erection. The central regulation of penile erection involves many transmitters, but their specific function is unknown [19,20]. Nerve impulses trigger neurotransmitters’ release and relaxing factors from the endothelial cells, resulting in smooth muscle cells’ Figure 1. Pathways of penile erection: Dilation of cavernosal arteries and smooth muscle cells (SMCs) of cavernosal spaces is mediated by the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway. NO is derived from nonadrenergic, noncholinergic nerves (nNOS, NOS type I), and the endothelium (eNOS or NOS type III) of cavernosal sinuses (both calcium2+/calmodulin-dependent isoforms). NO crosses plasma membranes to enter vascular smooth muscle cells (VSMCs) and promotes the synthesis and accumulation of cGMP, which induces a cascade reaction, leading to smooth muscle relaxation by reducing intracellular calcium levels. NNOS = neuronal nitric oxide. ENOS = endothelial nitric oxide. See the text for details.</strong></p><p><strong>[ATTACH=full]13869[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 200132, member: 13851"] [B]Figure 1. Pathways of penile erection: Dilation of cavernosal arteries and smooth muscle cells (SMCs) of cavernosal spaces is mediated by the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway. NO is derived from nonadrenergic, noncholinergic nerves (nNOS, NOS type I), and the endothelium (eNOS or NOS type III) of cavernosal sinuses (both calcium2+/calmodulin-dependent isoforms). NO crosses plasma membranes to enter vascular smooth muscle cells (VSMCs) and promotes the synthesis and accumulation of cGMP, which induces a cascade reaction, leading to smooth muscle relaxation by reducing intracellular calcium levels. NNOS = neuronal nitric oxide. ENOS = endothelial nitric oxide. See the text for details. A physiological penile erection requires normal vascular, neurological, and tissue responses. Penile erection is initiated after the central stimulus and integration of tactile, visual, olfactory, and imaginative triggers. Different observations demonstrate a network of afferent fibers from the genitals, spinal interneurons, and sympathetic, parasympathetic, and somatic nuclei, receiving stimulus from the periphery at the spinal cord level triggering reflexive erections. This network seems to receive also supraspinal information. At the level of the central nervous tissue, afferent data is processed in the forebrain and hypothalamus. In this latter area, the medial preoptic center, paraventricular nucleus, and anterior hypothalamic regions regulate erections and modulate autonomic events associated with sexual response. Different efferent pathways are present between the hypothalamus and sacral autonomic centers represented by the thoracolumbar and sacral autonomic nuclei. The erectile activity is finally coordinated by autonomic fibers network to the penis and somatic fibers pathways to the perineal striated muscles, responsible, in turn, for penis sensation. The cavernosal nerves originate from the autonomic system and are made of both sympathetic and parasympathetic fibers. These fibers travel along the prostate and enter the corpus spongiosum and the corpora cavernosa to regulate the blood flow during erection. The central regulation of penile erection involves many transmitters, but their specific function is unknown [19,20]. Nerve impulses trigger neurotransmitters’ release and relaxing factors from the endothelial cells, resulting in smooth muscle cells’ Figure 1. Pathways of penile erection: Dilation of cavernosal arteries and smooth muscle cells (SMCs) of cavernosal spaces is mediated by the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway. NO is derived from nonadrenergic, noncholinergic nerves (nNOS, NOS type I), and the endothelium (eNOS or NOS type III) of cavernosal sinuses (both calcium2+/calmodulin-dependent isoforms). NO crosses plasma membranes to enter vascular smooth muscle cells (VSMCs) and promotes the synthesis and accumulation of cGMP, which induces a cascade reaction, leading to smooth muscle relaxation by reducing intracellular calcium levels. NNOS = neuronal nitric oxide. ENOS = endothelial nitric oxide. See the text for details. [ATTACH type="full"]13869[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Anatomy, Pathophysiology, Molecular Mechanisms, and Clinical Management of ED in Patients Affected by CAD
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