Male Reproductive Physiology - pediagenosis
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Monday, October 8, 2018

Male Reproductive Physiology

Male Reproductive Physiology
Erection, emission and ejaculation
An erection is a complex neuropsychologic event. It occurs when blood rapidly flows into the penis and becomes trapped in its spongy chambers. The three systems directly involved in a penile erection are: (i) the spongy corpora cavernosa; (ii) the autonomic innervation of the penis; and (iii) the blood supply of the penis. Sensory, peripheral and central nervous system pathways integrate the response.

Although there are three erectile bodies within the penis, the two corpora cavernosa are primarily responsible for penile rigidity during an erection. The corpus spongiosum becomes tumescent during an erection, but does not become rigid. It serves to redistribute the intraurethral pressure so that the urethra remains patent and an effective conduit for the ejaculate.

The basic physiology of an erection is best understood if one considers each corpus cavernosum as if it were a single lacunar chamber (Fig. 13.1a). Small (helicine) arteries transmit blood into the lacunar space, which is bounded by smooth muscle within the trabecular wall. These arteries have rigid, muscular walls. Exiting from the lacunar space are small venules that coalesce into larger (subtunical) venules. The subtunical venules drain through the tunica albuginea and form the emissary veins. Unlike arteries, veins have very flexible walls and are readily compressed.
When the penis is flaccid, the smooth muscle in the lacunar walls is in a contracted state. This contracted state is maintained by noradrenergic sympathetic fibers. Noradrenergic tone is blocked upon activation of the parasympathetic system and the intralacunar smooth muscle relaxes. Blood flows easily into the relaxed lacunar space through the helicine arteries. This distends the lacunar space and the subtunical venules and emissary veins are physically compressed by the expanded lacunae. In essence, the lacunar space becomes a large vascular “sink.” Blood readily flows into this sink, but it is unable to exit via the penile venous system. Distension increases until the intralacunar pressure equals the mean arterial pressure.
Regulation of cavernosal smooth muscle is central to control of an erection. Simultaneous parasympathetic neural pathway activation and inhibition of sympathetic outflow are required for the smooth muscle relaxation that allows blood to flow into the sinusoidal spaces (Fig. 13.1b). The parasympathetic nervous innervation travels to the penis through the pelvic nerve whereas the sympathetic innervation travels in the hypogastric nerve. Numerous neurotransmitters are involved in the parasympathetic modulation of cavernosal smooth muscle relaxation. Nitric oxide is the primary proerectile neurotransmitter. It colocalizes with acetylcholine and vasoactive intestinal peptide (VIP) in nerve fibers terminating on the trabeculae of the corpora cavernosa and on the helicine arteries. Cavernosal smooth muscle contraction appears to be largely under α-noradrenergic control. Norepinephrine is the major antierectile agent.
Reflex erection can be elicited by afferent signals from sensory nerve endings on the glans; this reflex is mediated at the level of the spinal cord. The afferent limb of the reflex is carried by the internal pudendal nerves, which can also be activated by tactile stimulation of the perineum near the testes and scrotum. Erections can be modulated by supraspinal influences in the central nervous system. For instance, serotonergic pathways within the raphe nucleus of the midbrain can inhibit erections. The amygdala and the medial preoptic area of the hypothalamus appear to be important higher integrating centers in the modulation of erection. Dopamine is the candidate neurotransmitter in erectile control at this level.
The importance of testosterone in erectile function is not known. Nocturnal erections, which occur during episodes of rapid eye movement (REM) sleep, are testosterone dependent. In contrast, erections that occur in response to visual stimuli are not dependent on testosterone and will occur in hypogonadal men.
As ejaculation approaches, penile turgor increases even more. The smooth muscles in the prostate, vas deferens and seminal vesicles contract sequentially to expel the seminal plasma and spermatozoa into the urethra in a process known as emission. Emission is mediated by α-adrenergic sympathetic fibers that travel through the hypogastric nerve. Although emission and ejaculation are sometimes discussed as a single entity under the term ejaculation, these processes are distinct; ejaculation describes the ejection of semen from the posterior urethra. Ejaculation requires contraction of the smooth muscles of the urethra and the striated bulbocavernosus and ischiocavernosus muscles. These contractions are controlled through a spinal reflex mediated by the pudendal nerve and spinal nerves 2, 3 and 4 (Table 13.1).

Hormonal control of spermatogenesis Although ongoing spermatogenesis in the testes can be maintained qualitatively by testosterone alone, follicle-stimulating hormone (FSH) is required for initiation of spermatogenesis. The primary site of action of FSH within the seminiferous epithelium is in the Sertoli cells. FSH is delivered to the interstitial area of the testis via small arterioles. Once there, it diffuses through the basement membrane of the seminiferous tubules and binds to specific plasma membrane receptors on Sertoli cells. Activation of the FSH receptors results in the synthesis of both intracellular androgen receptors and androgen- binding protein (ABP). ABP is secreted from the Sertoli cells and binds androgens that have been produced by Leydig cells and diffused from their interstitial site of production into the seminiferous tubule. ABP transfers these androgens to the germ cells. Here, the androgens will be retained in the promeiotic germ cells that contain androgen receptors. Once FSH initiates spermatogenesis, the process will proceed as long as an adequate and uninterrupted supply of testoster- one is available.
The FSH dependence of the Sertoli cells is analogous to the FSH control of the homologous granulosa cells in the ovary. Like follicular phase ovarian granulosa cells, Sertoli cells also secrete inhibin and activin. Inhibin, along with testosterone, inhibits pituitary FSH secretion in the male. Activin receptors have been identified on spermatogenic cells and may be involved in the FSH-mediated initiation of spermatogenesis.

Leydig cell function
Like the homologous theca cells in the ovary, Leydig cells respond to luteinizing hormone (LH) by synthesizing and secreting testosterone in a dose-dependent manner. In addition to LH receptors, receptors for prolactin and inhibin are found on Leydig cells. Both prolactin and inhibin facilitate the stimulatory activity of LH on testosterone production; neither can do this in isolation.

Regulation of gonadotropin secretion in males
The neuroendocrine mechanisms that regulate testicular function are fundamentally similar to those that regulate ovarian function. Hypothalamic gonadotropin-releasing hormone (GnRH), secreted in a pulsatile fashion into the pituitary portal system, acts on the pituitary of the male to stimulate synthesis and release of the gonadotropins, FSH and LH (Chapter 1). These two gonadotropins regulate the spermatogenic and endocrine activities of the testis. The male and female utilize the same negative feedback mechanisms to inhibit gonadotropin release by the pituitary. However, there is a major difference between regulation of the male and female hypothalamic–pituitary–gonadal systems. The postpubertal male has continuous gametogenesis and testosterone production while the postpubertal female has cyclic functions. The lack of cyclicity in males occurs because androgens do not exert a positive feedback on gonadotropin release.
Testosterone is the major regulator of LH secretion in the male. The negative feedback effect of testosterone is achieved largely by decreasing the frequency of the GnRH pulses released by the hypothalamus; although there are minor reductions in GnRH pulse amplitude. Testosterone also inhibits FSH release but its effects are not as pronounced as they are on LH. Combinations of testosterone and the Sertoli cell hormone inhibin are required to produce maximal FSH suppression.

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