Review of the Male Reproductive System

Core Concepts

Anatomy: the organs and their jobs

• Testes. Two functions in one organ: the seminiferous tubules produce sperm, with support from Sertoli cells; the Leydig cells in the tissue between tubules produce testosterone.
• Epididymis. A coiled duct on each testis where sperm mature and are stored; sperm leave the testis immotile and gain motility and fertilizing ability here.
• Vas deferens. The muscular duct that propels sperm during ejaculation.
• Seminal vesicles. Paired glands that produce most of the ejaculate volume, including fructose, an energy source for sperm.
• Prostate. A walnut-sized gland surrounding the urethra; it secretes fluid containing prostate-specific antigen (PSA) and zinc, and it is the site of benign prostatic hyperplasia.
• Bulbourethral (Cowper's) glands. Small glands that add lubricating mucus to the ejaculate.
• Penis. Contains erectile tissue: two corpora cavernosa and the corpus spongiosum, which fill with blood during erection.

The hypothalamic-pituitary-gonadal (HPG) axis

The hypothalamus releases gonadotropin-releasing hormone (GnRH) in pulses. GnRH travels to the anterior pituitary, which responds by releasing two hormones:

• Luteinizing hormone (LH) → stimulates Leydig cells → testosterone production.
• Follicle-stimulating hormone (FSH) → acts on Sertoli cells → supports spermatogenesis (working together with testosterone).

The loop closes with negative feedback: testosterone inhibits GnRH and LH release, and inhibin — a hormone secreted by Sertoli cells — inhibits FSH. The result is a self-regulating system. Two practical implications matter for pharmacology: (1) exogenous testosterone suppresses the axis, so sperm counts fall and testes shrink; (2) drugs that disrupt GnRH or LH signaling can shut down testosterone production — the basis of androgen deprivation therapy in Topic 6.

Testosterone: the master androgen

An androgen is any steroid hormone with masculinizing effects; testosterone is the principal one. In fetal development it masculinizes the internal genital tract (DHT is needed for the external genitalia). At puberty it drives voice deepening, genital growth, pubic and axillary hair, muscle and bone mass, and the growth spurt. In adulthood it maintains libido, spermatogenesis, muscle and bone mass, red blood cell production (it stimulates erythropoietin), and mood and energy.

In the blood, testosterone is mostly bound to carrier proteins (sex hormone-binding globulin and albumin); the small free fraction is the active one. Two conversions shape its effects:

• 5-alpha-reductase converts testosterone to dihydrotestosterone (DHT) in the prostate and skin — DHT drives prostate growth and facial/body hair (Topics 6 and 8).
• Aromatase converts some testosterone to estradiol in adipose and other tissues — which is why androgen excess can cause gynecomastia.

Spermatogenesis and the Sertoli cell

Sperm develop continuously from puberty in the seminiferous tubules, taking roughly two months per cycle. The scrotum keeps the testes cooler than core body temperature, which spermatogenesis requires. Sertoli cells line the tubules: they nourish developing sperm, form the blood-testis barrier, and secrete inhibin. Sperm that leave the testis are immotile; they mature in the epididymis. Semen is mostly accessory-gland fluid, not sperm: a small fraction of the volume is sperm; the rest is seminal vesicle fluid (fructose, prostaglandins), prostatic fluid (PSA, zinc, enzymes), and mucus.

Erection and ejaculation: the neural and vascular basis

Erection is a vascular event driven by the parasympathetic system. Sexual stimulation triggers release of nitric oxide (NO) in the corpora cavernosa; NO activates guanylate cyclase, which produces cyclic GMP (cGMP); cGMP relaxes cavernosal smooth muscle, the erectile tissue fills with blood, and the veins are compressed, producing a rigid erection. The enzyme phosphodiesterase 5 (PDE5) degrades cGMP and returns the tissue to flaccidity — exactly the target of PDE5 inhibitors in Topic 7.

Ejaculation is a sympathetic event: contraction of the epididymis, vas deferens, seminal vesicles, and prostate propels semen forward while the bladder neck closes so semen does not travel backward. Alpha-1 receptors on prostate and bladder-neck smooth muscle participate in this process — which is why alpha blockers can cause retrograde ejaculation (Topic 8).

Aging changes

Testosterone levels decline gradually with age; erectile function increasingly reflects vascular health; and the prostate enlarges in most men, so BPH compresses the urethra and causes lower urinary tract symptoms (Topic 8). These changes are normal, but their consequences are treatable — the reason the rest of this chapter exists.

Common Confusions