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Structure of the Male Reproductive System

Paper Type: Free Essay Subject: Biology
Wordcount: 5442 words Published: 12th Mar 2018

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New chapter 35

The Male Reproductive System


The male reproductive system has three principal functions:

  1. The differentiation and maintenance of the primary and secondary sex characteristics under the influence of the hormone testos­terone, made in the testes.
  2. Spermatogenesis—the creation of the male gametes inside the testes.
  3. The penile delivery of sperm from the testes into the female’s vagina in the act of procre­ation. This includes penile erection and ejaculation.


The male reproductive system comprises not only the male genitals, but also the cranial structures that help regulate the performance of the male re­productive system—namely, the hypothalamus and pituitary. At the hypothalamic and pituitary level, however, male and female anatomy and histology are more or less the same. For more details on the hy­pothalamic and pituitary structures involved in hu­man reproduction, see Chapter 36. In the section that follows, we will focus on the anatomy and histology of the testes, the penis, and the ductal connections between the testes and penis.

The Testes

The male gonads, or testes, are suspended from the perineum in an external contractile sac called the scrotum (Figure 37.1A). Each testis is about 4 cm long, and the testes are perfused by the spermatic arteries. The spermatic arteries are closely apposed with the spermatic venous plexus, and this close contact al­lows countercurrent heat exchange between artery and vein, cooling the blood that flows to the testes. Countercurrent heat exchange helps keep the testic­ular temperature cool enough for optimal spermato­genesis (1°C to 2°C cooler than body temperature). The external location of the testes in the scrotum serves as a second important cooling mechanism. Because the testes develop within the abdomen, they descend into the scrotum during fetal life, reaching the deep inguinal rings around week 28 of gestation and inhab­iting the scrotum by birth. In some instances (3% of the time in full-term male infants), the testes do not descend—a condition called cryptorchidism. Cryp­torchidism must be corrected if the male is to have properly functioning, fertile gonads.

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The testes are composed of coiled seminiferous tubules embedded in connective tissue (see Figure 37.1B). The connective tissue, which makes up about 20% of the testicular mass, contains Leydig cells, which make testosterone. The seminiferous tubules, constituting 80% of the testicular mass, generate the sperm. The tubules contain two main cell types: spermatogonia and Sertoli cells. Sper­matogonia are the germ cells that undergo meiosis to give rise to spermatids, the immediate precursors to spermatozoa. The copious cytoplasm of the Sertoli cells completely envelops and protects the spermatids, sealing them off from any contact with the tubules’ outer basement membrane or blood supply. This Sertoli sheath hence forms a blood-testis barrier to protect the male gametes from any harmful bloodborne agents, and to prevent the immune system from attacking the unique sperm-specific proteins as though they were foreign anti­gens. By virtue of their position between the blood and the spermatids, the Sertoli cells also transport nutrients, oxygen, and hormones, such as testos­terone, to the spermatids.

Figure 37.1 Anatomy of the male reproductive system. A. Overview. B. A closer look at the testis. C. The ducts of the reproductive system shown in isolation. The ducts arising from both testes are depicted, converging on the posterior urethra inside the prostate gland.

The spermatogonia sit outside the blood-testis barrier near the basement membrane. Here, they continuously conduct mitosis. The products of mitosis are pushed toward the tubule lumen and undergo meiosis and differentiation into sperm cells. The Sertoli barrier is fluid and accommodates the passage of cells developing into spermatids. The testes make around 120 million sperm a day. As they differentiate, the sperm migrate into the tubule lu­men for transport distally to the rete testis, a plexus of ducts that collects sperm from each of roughly 900 seminiferous tubules. The rete testis empties into the epididymis, a single coiled tubule running from the top of the testis down its posterior aspect. In the epididymis, sperm are stored and undergo maturation before continuing their voyage outside the testis.

The Ducts and Penis

Each epididymis leads to a long, straight tube called the vas deferens (see Figure 37.1C). The vas deferens from the epididymis of each testis rises in the scrotum, ranges laterally through the inguinal canals, runs along the pelvic wall toward the poste­rior, and descends along the posterior aspect of the bladder. Here the two vas deferens tubes widen into ampullae, which are attached to glands called the seminal vesicles. (There are two seminal vesicles, one for each vas deferens.) The seminal vesicles se­crete more than half the volume of the semen. The two ampullae each send an ejaculatory duct through the prostate gland, and the ejaculatory ducts join the urethra inside the tissue of the prostate gland. From this point onward, the male urethra serves as part of both the reproductive and urinary tracts, unlike female anatomy, in which the reproductive and urinary tracts are completely separate. Male physiol­ogy ensures that micturition and ejaculation do not occur simultaneously.

The urethra next passes through the muscle tissue of the urogenital diaphragm, a consciously controllable sphincter. Sitting just under the urogen­ital diaphragm are the bulbourethral glands (also called Cowper’s glands), which lubricate the urethra with mucus. Finally, the urethra enters the penis. The cylindrical penis houses the urethra in erectile tissue, which helps effect the transition between the excretory and reproductive functions of the urethra (Figure 37.2). This erectile tissue contains cavernous sinuses that fill with blood under circumstances of increased penile blood flow, leading to erection of the penis. When erect, the penis may be inserted into the vagina so that sperm may be delivered to the fallop­ian tubes.

Figure 37.2 Cross-section of the penis.

The erectile tissue is present in three cylinders inside the penis, each called a corpus cavernosum and together called the corpora cavernosa. Two of the corpora lie dorsally and are sheathed by the ischio­cavernosus muscles. One lies ventrally and is sheathed by the bulbospongiosus muscle. The ventral corpus cavernosum is also called the corpus spongiosum, and it is special in that it contains the urethra and forms the glans penis, the spongy head of the penis. The corpora are each supplied by a cavernous artery that gives out helicine arteries. The penis averages 8.8 cm (3.5 in) in length when flaccid and 12.9 cm (5.1 in) when erect, indicating no correlation between flaccid and erect size.


Just as the female reproductive system is coor­dinated by the hypothalamus and pituitary, the activities of the male reproductive system are coor­dinated by the HPG axis, in this case the hypothala­mic-pituitary-testicular (HPT) axis (Figure 37.3). (The gonadal HPT axis is not to be confused with the hy­pothalamic-pituitary-thyroid axis, also labeled HPT.) The male axis shares with the female the exact same hypothalamic hormone, gonadotropin- releasing hormone (GnRH), and the same pituitary go­nadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). (The gonadotropins are named for their female reproductive functions, but they act in the male nonetheless.) The same array of gonadal steroid hormones that is produced by the ovary is also synthesized by the male reproductive system, but in different proportions. Because of differential expression of enzymes in the steroid synthesis pathway, the female gonad makes predom­inantly progesterone and estrogen, while the male gonad predominantly makes the androgen steroid hormone testosterone. Testosterone inhibits the secretion of GnRH, LH, and FSH in a classic negative-feedback loop.

Figure 37.3 Hypothalamic-pituitary-testicular axis. Plus signs represent stimulation; minus signs represent inhibition.

The HPT Axis

GnRH is the initial driver of testicular function. It is secreted in a pulsatile fashion (one pulse every 1 to 3 hours) and distributes to the pituitary gonadotrophs through the hypothalamic-pituitary portal circula- tion. There, the releasing hormone stimulates the LH- and FSH-secreting cells. Each GnRH pulse directly prompts an LH pulse from the gonadotrophs. More frequent or larger-amplitude GnRH pulses result in more frequent or larger-amplitude LH pulses. GnRH also increases FSH release, but the correlation between GnRH and FSH release is not as exact.

LH acts on the Leydig cells. The LH signal is transduced by a seven- transmembrane receptor linked through a G protein to adenylyl cyclase, which produces cAMP. LH-dependent elevations in cAMP promote testosterone synthesis from cholesterol and promote the growth of Leydig cells. Testosterone synthesis is increased by the activation and increased expression of key proteins involved in steroidogenesis, such as the steroidogenic acute regu­latory protein (StAR). StAR shuttles cholesterol into steroid-manufacturing cells. The Leydig cells of the testis are unique in their ability to make testosterone in large amounts (Figure 37.4). While the zona reticulata cells of the adrenal gland also make androgens, the adrenal pathway stops at androstenedione, the im­mediate precursor to testosterone. (Some peripheral tissues can make testosterone from androstenedione in small amounts.)

FSH, meanwhile, binds to receptors on the Sertoli cells, activating the production of proteins involved in spermatogenesis. FSH also stimulates glucose metabolism, thereby providing energy to the sperm precursors. (Spermatogenesis will be discussed in more detail below.) Finally, FSH upregu­lates the expression of the androgen receptor in Sertoli cells, thereby potentiating the influence of testosterone upon spermatogenesis.

Like all steroids, testosterone binds an intracel­lular receptor, which binds DNA transcription factors and influences gene expression. The distribution of testosterone receptors in the body tissues deter­mines the targets of testosterone action. In addition, target tissues express an enzyme that converts testos­terone to its more active form, dihydrotestosterone (DHT). This enzyme is 5-reductase. DHT binds more avidly to the androgen receptor than does testos­terone itself. Testosterone from the Leydig cells passes through the Sertoli cells and into the seminif­erous tubules, where, alongside FSH, it promotes spermatogenesis. The Sertoli cells make androgen-binding protein (ABP), which helps them to retain testosterone. Testosterone also acts systemically, promoting growth and sustaining gene expression in many peripheral tissues. Testosterone is transported in the blood by sex hormone-binding protein (SHBP), also called sex hormone-binding globulin, a liver-produced carrier protein that is structurally similar to ABP. It is thought that testosterone and SHBP itself may act at cell membrane receptors, in addition to testosterone’s genomic effects. This is parallel to the genomic and nongenomic modes of signal transduc­tion employed by thyroid hormone.

Finally, testosterone inhibits GnRH and go­nadotropin secretion. Thus, testosterone limits its own production and action. Inhibin from the Sertoli cells also inhibits the pituitary and hypothalamus. Inhibin is a TGF- glycoprotein hormone. Investiga­tions suggest that additional feedback mechanisms link Sertoli cell behavior with Leydig cell behavior. Table 37.1 summarizes the actions of testosterone.

Table 37.1 Testosterone Actions

Causes and sustains expression of the male sex characteristics:

Embryologic development of male genitals and ducts

Growth of penis, testes, and prostate at puberty

Growth of hair, larynx

Promotion of positive nitrogen balance in muscles, bones, and skin (promotion of increased protein anabolism, requiring retention of more nitrogen-containing amino acids)

Increased libido and aggression

Causes spermatogenesis

Inhibits HPT axis (negative feedback)

The Expression of Male Sex Characteristics

The male reproductive system begins to function during embryonic life. As soon as the testes form and are capable of secreting testosterone, the androgen begins to act on the body tissues. At this stage, the hormone differentiates the fetus into a male with the appropriate primary sex characteristics—the male genitals. At puberty, testosterone causes sustained expression of the secondary sex characteristics, which are gender-based phenotypes other than the genitals, such as hair growth, muscle development, and a low voice.

Fetal Life and Infancy (Primary Sex Characteristics) While the testes do act in utero, they cannot act before they have formed, and they do not form right away. In fact, before 6 weeks of gestation, the gonads of geno­typically male or female embryos have not begun to differentiate into either ovaries or testes. The so-called “indifferent gonad” has an inner medullary (male) and an outer cortical (female) layer. In addition, the anatomic precursors of both males (the Wolffian ducts) and females (the Müllerian ducts) are present. Only at 6 to 8 weeks of gestation is male sexual devel­opment initiated by the SRY gene, a gene on the short arm of the Y chromosome. SRY encodes a zinc finger DNA-binding protein called testis determining factor (TDF). Under the influence of TDF, the medullae of the indifferent gonads develop while the cortices regress. The previously indifferent gonads differentiate into testes: embryonic germ cells form spermatogonia, coelomic epithelial cells form Sertoli cells (6 to 7 weeks of gestation), and mesenchymal stromal cells form Leydig cells (8 to 9 weeks of gestation).

Now the testes can begin to act. The Sertoli cells secrete a Müllerian-inhibiting factor (MIF), which causes regression of the Müllerian ducts. Human chorionic gonadotropin (hCG)—which is structurally related to LH—stimulates the Leydig cells to prolifer­ate and secrete testosterone. The testosterone is reduced to DHT in target tissues by 5-reductase. As long as target tissues contain the androgen receptor and 5-reductase, DHT induces those tissues to form the primary male sex characteristics, the male repro­ductive organs. Under the influence of DHT, the Wolffian ducts differentiate into the epididymis, vas deferens, and seminal vesicles. The genital tubercle transforms into the glans penis, the urethral folds grow into the penile shaft, and the urogenital sinus becomes the prostate gland. Finally, DHT causes the genital swellings to fuse, forming the scrotum.

At its peak, the fetal testosterone level reaches 400 ng/dL, but by birth it falls below 50 ng/dL. There is a brief spike in the male infant’s testosterone level between 4 and 8 weeks after birth, but its function is not well understood. Otherwise, the testosterone level remains low throughout childhood, until puberty.

Puberty and Beyond (Secondary Sex Characteristics) Puberty is the process by which males and females achieve reproductive capacity, and it begins in both sexes with an increase in hypothalamic GnRH secre­tion. It is possible that this increase is in response to decreasing hypothalamic sensitivity to testos­terone’s negative-feedback effects. As the child ap­proaches adolescence, the hypothalamus gradually escapes inhibition and GnRH secretion rises. LH and FSH secretion in turn rise, and testosterone secretion from the testes increases. Gradual maturation of hypothalamic neurons probably plays a role in this pubertal change in GnRH secretion.

Increased testicular production of testosterone and other androgens at puberty has a host of effects. The earliest one is enlargement of the penis and testes. From the beginning to the end of puberty, the testicular volume more than quadruples. Spermato­genesis commences (with testosterone effects per­haps being most important on the spermatids), and the prostate gland is stimulated to grow. Growth oc­curs in many tissues outside the reproductive system as well.

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Androgens are anabolic steroids; they promote the storage of energy in complex molecules. While an­drogens promote protein synthesis, an anabolic hor­mone like insulin has a greater effect on the formation of complex carbohydrates and fats. Increased protein synthesis is associated with the growth of skeletal muscle, bones, skin, and hair (pubic, axillary, facial, chest, arms, and legs) and the growth of the larynx (which deepens the voice and causes the thyroid car­tilage, or Adam’s apple, to protrude). Men on average have around 50% more muscle mass than women; they have stronger, denser bone matrices and thicker skin. Muscle does not contain 5-reductase, so it ap­pears that testosterone, not DHT, promotes muscular protein anabolism. However, testosterone or DHT may promote muscular anabolism via extramuscular effects, such as the stimulation of growth hormone and insulin-like growth factor (IGF-1) production.

Collectively, the development of the secondary sex characteristics is called virilization (after the Latin vir for man). It appears that while testosterone promotes all of these effects—genital growth and spermatogenesis, hair growth, behavioral changes, and anabolism in peripheral tissues—certain andro­gen precursors, metabolic byproducts, and pharma­ceutical androgen analogs preferentially serve peripheral anabolism. Many of these metabolites and drugs are abused by bodybuilders and athletes. (See Clinical Application Box The Use and Abuse of An­abolic Steroids.)

Testosterone, combined with a genetic predis­position, also influences hair growth on the head. Male-pattern baldness typically begins with a de­crease in hair growth on the top of the head and progresses to a complete lack of hair growth extend­ing from the top of the head down. Both factors, the androgens and the genes, are necessary for baldness to occur; a man without the genetic predisposition will not become bald regardless of his testosterone level. A woman with the genetic predisposition will usually not become bald unless she suffers from excess androgen production. Similarly, a castrated male with low testosterone levels will not become bald even if he has a genetic predisposition.

Once testosterone levels rise during puberty, they reach a plateau and remain elevated until a man reaches his seventies, when they begin to decline. This event, called the male climacteric, may create some symptoms resembling those of female menopause. However, hormone replacement therapy (HRT) is not commonly used to treat these symp­toms. One reason is that men in this age group are at increased risk for prostate cancer. Because testos­terone has proliferative effects on the prostate, HRT might further increase the risk of prostate cancer. While testosterone does promote spermatogenesis, this testicular function is remarkably well preserved in men even after the climacteric.

The Haploid Life Cycle in the Male

As mentioned above, spermatogenesis begins with puberty and continues into the eighth decade of life. Spermatogenesis has three phases: sperma­tocytogenesis, during which the primordial sper­matogonia divide by mitosis and differentiate into spermatocytes; meiosis, resulting in four haploid gametes called spermatids, each with a quarter of the cytoplasm of the original spermatogonium (see Chapter 36); and spermiogenesis, during which the spermatids are nourished and physically reshaped by the surrounding Sertoli cells. The product of spermiogenesis is spermatozoa, or sperm (Figure 37.5). After spermiogenesis, the epididymis and repro­ductive tract glands help prepare the sperm for fertilization.

Spermatocytogenesis and Meiosis The evolving group of cells spanning from spermatogonia to sper­matozoa is sometimes called the spermatogenic series. Not all spermatogonia enter into the sper­matogenic series. If they did, they would be con­sumed—as happens to the oogonia in the ovary, eventually leading to menopause. Instead, the testis csontinually replenishes its own supply of spermato­gonia. As they undergo mitosis, some of the new ones are committed to the spermatogenic series, while some remain undifferentiated. The undifferen- tiated stem cells are called type A spermatogonia, and the differentiated spermatogonia committed to becom­ing spermatocytes are called type B spermatogonia.

Once this allocation of mitotic products into one group or another occurs, spermatocytogenesis con­tinues as follows. Type A spermatogonia remain on the outside of the blood-testis barrier, while type B spermatogonia cross it, becoming enveloped by the cytoplasmic processes of the Sertoli cells. These type B spermatogonia differentiate further and enlarge to become primary spermatocytes. The primary sperma­tocytes then enter meiosis, a process that takes around 3.5 weeks to complete, almost all of which is spent in prophase (when the newly replicated chro­mosomes condense). Each primary spermatocyte di­vides into two secondary spermatocytes, which in turn divide again into a total of four haploid spermatids. Each spermatid contains either an X chromosome or a Y chromosome. The male’s gamete thus decides the sex of his offspring.

Spermiogenesis Spermiogenesis begins once the spermatids are created and delivered into the em­brace of the amoeboid Sertoli cells (Figure 37.6). The spermatid elongates and reorganizes its nuclear and cytoplasmic contents into a spermatozoon with a dis­tinct head and tail. The head consists of a condensed nucleus surrounded by a thin layer of cytoplasm. The rest of the retained cytoplasm and cell membrane is shifted toward the opposite end of the sperm, the tail. A large amount of the spermatid’s cytoplasm is shed into the surrounding Sertoli cell during spermiogene­sis. As the transformed sperm is extruded into the seminiferous tubule lumen, the discarded cytoplasm remains embedded in the cytoplasm of the Sertoli cell, where it is ultimately phagocytized.

Figure 37.6 Spermiogenesis

The structure of sperm cells enables them to swim up the female reproductive tract and fertilize oocytes. The tail of a sperm contains a flagellum for motility. Originating from one of the centrioles of the sperm cells, the flagellum consists of a central skele­ton of microtubules called the axoneme. The axoneme is arranged in the ancient 9 + 2 pattern characteristic of eukaryotic cilia and flagella across all kingdoms and phyla of life: 9 pairs of microtubules surrounding 2 central tubules, linked via a complex array of protein bridges. The sperm cell’s mitochondria aggregate along the proximal end of the flagellum and supply energy for movement to the flagellum. The flagellum enables the sperm to swim.

The anterior two thirds of the head of the sperm cell is surrounded by a thick capsule known as the acrosome, formed from the Golgi apparatus. The Golgi apparatus contains numerous hydrolytic and proteolytic enzymes, similar to those found in lysosomes, and ultimately facilitates the sperm’s penetration of the egg for fertilization. There is also evidence to suggest a role for the acrosomal enzymes in penetrating the mucus of the female cervix.

Epididymal Sperm Maturation and Storage After spermiogenesis is complete, the sperm pass out of the testis (through the rete testis) and into the epi­didymis, where growth and differentiation continue. After the first 24 hours in the epididymis, the sperm acquire the potential for motility. However, the epithelial cells of the epididymis secrete inhibitory proteins that suppress this potential. Thus, the 120 million sperm produced each day in the seminiferous tubules are stored in the epididymis, as well as in the vas deferens and ampulla. The sperm can remain in these excretory genital ducts in a deeply suppressed and inactive state for over a month without losing their potential fertility.

The epididymis also secretes a special nutrient fluid that is ultimately ejaculated with the sperm and is thought to mature the sperm. This fluid contains hormones, enzymes (such as glycosyltransferases and glycosidases), and nutrients that are essential to achieving fertilization. The precise function of many of these factors is not known, but enzymes like gamma-glutamyl transpeptidase are thought to serve as antioxidants defending against mutations in the sperm.

Potentiation in the Ejaculate The accessory genital glands—the seminal vesicles, prostate gland, and bulbourethral glands—also contribute to potentia­tion. During ejaculation, their secretions dilute the epididymal inhibitory proteins, allowing the sperm’s motile potential to be realized. In addition, the glands make individual contributions to sperm preparation and support. The seminal vesicles secrete semen, a mucoid yellowish material containing nutrients and sperm-activating substances such as fructose, cit­rate, inositol, prostaglandins, and fibrinogen. Carbo­hydrates such as fructose provide a source of energy for the sperm mitochondria as they power the sperm’s flagellar movements. The prostaglandins are believed to aid the sperm by affecting the female gen­ital tract—making the cervical mucus more receptive to the sperm, and dampening the peristaltic contrac­tions of the uterus and fallopian tubes to prevent them from expelling the sperm.

The prostate gland secretes a thin, milky, and al­kaline fluid during ejaculation that mixes with the contents of the vas deferens. The prostatic secretion contains calcium, zinc, and phosphate ions, citrate, acid phosphatase, and various clotting enzymes. The clotting enzymes react with the fibrinogen of the seminal fluid, forming a weak coagulum that glues the semen inside the vagina and facilitates the passage of sperm through the cervix in larger numbers. The al­kalinity imparted to semen by the prostate counter­acts vaginal acidity, which is a natural defense against microbial pathogens and which can kill sperm or impair sperm motility. By titrating the acid­ity, the prostate ensures that the sperm can elude this antimicrobial defense.

Capacitation in the Female Reproductive Tract Ejaculated sperm is not immediately capable of fertilizing the female oocyte. In the first few hours after ejaculation, the spermatozoa must undergo capacitation inside the female reproductive tract. This is the final step in preparation for fertilization. First, the fluids of the female reproductive tract wash away more of the inhibitory factors of the male geni­tal fluid. The flagella of the sperm hence act more readily, producing the whiplash motion that is needed for the sperm to swim to the oocyte in the fallopian tube. Second, the cell membrane of the head of the sperm is modified in preparation for the ultimate acrosomal reaction and penetration of the oocyte. Capacitation is an incompletely understood phenomenon.

Fertilization Once capacitated, the spermatozoa travel to the oocyte. There is an enormous rate of at­trition among the hundreds of millions of ejaculated sperm, and at most a few hundred reach the oocyte. However, the female reproductive tract is simultane­ously increasing receptivity to the male gametes (see Chapter 36).

When the few hundred sperm reach the egg, they begin to try to penetrate the granulosa cells surrounding the secondary oocyte. The sperm’s acrosome contains hyaluronidase and proteolytic enzymes, which open this path. As the anterior mem­brane of the acrosome reaches the zona pellucida (the glycoprotein coat surrounding the oocyte), it rapidly dissolves and releases the acrosomal enzymes. Within minutes, these enzymes open a pathway through the zona pellucida for the sperm cytoplasm to merge with the oocyte cytoplasm. From beginning to end, the process of fertilization takes about half an hour.

Figure 37.7 Sexual response and changes in the penis.

Penile Erection and Ejaculation

The practice of internal fertilization, in which the male deposits gametes directly into the reproductive tract of the female, is at least 300 million years old. Early cartilaginous fishes probably were its innova­tors. These elasmobranchs retained their concepti internally until the eggs could be waterproofed and thus protected from the osmotic stress of seawater. Eventually, almost all the higher vertebrates would practice internal fertilization for the sake of defending the next generation.

For this reason, the male vertebrate possesses a special apparatus for penetrating the body of the female and delivering semen to an internal location. There are two physiologic events crucial to this in­ternal delivery of semen: penile erection, which makes it possible for the penis to penetrate the vagina, bringing the urethral opening, or meatus, into close contact with the female cervix; and ejaculation, in which the semen is secreted into the male repro­ductive ductal system, mixed with sperm, and then mechanically squirted out of the penis. Both of these events are initiated and controlled by the nervous system in connection with the subjective state of sexual arousal.

Sexual Response in the Male William H. Masters and Virginia E. Johnson in 1966 described four phases of sexual response


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