Hypogonadism, post-testicular sperm transit and modification, erectile dysfunction, reflexive pathways for erection, regulation of erection and ejaculation, ejaculatory dysfunction, disorders of the penis and urethra

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Colorado State University
Biomedical Science
BMS 460
D.Rao Veeramachaneni

6 December Testicular Dysfunction: Hypogonadism Follicle-stimulating hormone and testosterone are needed for spermatogenesis Either testosterone deficiency or defective spermatogenesis Oligospermia or azoospermia Manifestations of T deficiency vary with time of onset Due to lesions in Hypothalamus or anterior pituitary Tertiary/secondary or hypogonadotropic hypogonadism Testes Primary or hypergonadotropic hypogonadism A variety of toxicants/environmental factors target different phases of spermatogenesis Spermatogonium → spermatocyte Radiation and chemotherapeutic drugs block mitosis or may cause mutations Small adverse effects here can cause a large reduction in the sperm count Exposure to a range of environmental factors (chemicals/heat) can destroy some spermatocytes A normal man produces >100 million sperm every day. Each has taken 10 weeks to make Most environmental factors which impair spermatogenesis also inhibit normal sperm release; e.g., water disinfection by-products By systematic collection of seminal ejaculates, one can identify the interval between a detrimental event and a decline in sperm output Post-testicular Sperm Transit and Modifications In testis – sperm production Infertile/immotile entering epididymis In epididymis – sperm maturation, acquire ability to move and fertilize Seminal vesicle – fluid rich in fructose; 60% of ejaculate Prostate gland – fluid rich in citrate and other electrolytes; 30% of ejaculate Bulbourethral gland – fluid rich in mucus; 5% of ejaculate Erectile Dysfunction Psychogenic Neurologic Pudendal neuropathy, as in diabetes mellitus Vascular Obstructive arteriosclerosis, as in diabetes mellitus Hormonal Endocrinopathy Sympathetic, parasympathetic, and somatic nerves contribute to the male sexual response Direct autonomic input from pelvic plexus Somatic neural input from pudendal nerve Reflex pathways for erection Nitric oxide, a vasodilator, is the most important neurotransmitter to the arteries in this reflux Erection is mediated by the pelvic parasympathetic nerves. The initiation of an erection depends on the NANC (non-adrenergic, non-cholinergic) branch of parasympathetic nerves. Both NANC and acetylcholine (ACh) neurotransmitters stimulate nitric oxide (NO) release (ACh activates NO synthase) causing a cGMP-mediated smooth muscle relaxation. The relaxation allows an increase in blood flow and engorgement of the tissue. Descending CNS pathways triggered by thoughts, emotions, and sensory inputs such as sight and smell; input from penis mechanoreceptors → ↑ activity of neurons that release nitric oxide, ↓ activity of sympathetic neurons → dilation of arteries → erection → compression of veins Compression of veins → erection ED drugs inhibit degradation of cGMP by phosphodiesterase enzymes. Sildenafil is a phosphodiestase-5 inhibitor used to treat erectile dysfunction (ED). The dilation of vascular smooth muscle required to achieve an erection is mediated by NO and the intracellular second messenger cGMP. cGMP is broken down by phosphodiesterase. Consequently, inhibition of p
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