Physiology of the male reproductive
system
D. Gehan Shaker
Badawi
(2015) – (2016)
Specific objectives
At the end of this session, you should be able
to:
1. Mention cell types of the testis
2. Mention the functions of Sertoli cells
3. List hormones involved in gametogenesis
and steroidogenesis.
4. List hormones produced by the testis &
describe their functions
5. Discuss biological effects of androgen
(prenatal and postnatal effect).
6. Explain the mechanism of erection.
Male Reproductive System
Male Reproductive System
1ry sex organ
Testes
2ry sex organs
Tubular System
Glandular System
1. Gametogenesis
2. Steriodogenesis
Epididymis
Seminal vesicles
Secretes mucoid
viscid fluid rich in
Fructose, PGs,
ascorbic acid &
Fibrinogen
A single coiled
Prostate
tube that 
essential for
Secretes
thin milky
Motility and
mucous
alkaline fluid
Maturation of
contains
the sperms
plasmin, buffers,
Hyaluronidase
Cholesterol
Bulbourethral
Vas deference
Essential for:
Storage of
sperms (in its
ampulla)
Transports of
sperms to
ejaculatory
ducts.
The testes:

Represent 1ry sex organs in male

Have 2 main functions:
Spermatogenesis
i.e. formation of mature
sperms.
Steroidogenesis
i.e. synthesis and secretion of
male sex hormones (testicular
androgens)
Histologically
Spermatogenic cells
Formation of
mature sperm
Sortoli cells
1. Supportive
2. Protective
3. Nutritive Cells
Leydig Cells
Androgens
Secretion
Cells of the Testis
Spermatocytes
Sortoli cell
Leydig cell
Cells of the testis
Sertoli
cell
Leydig Cells
Hormonal Control of testicular cells
Hypothalamus
-ve feedback
GnRh
-ve feedback
Mainly inhibits FSH
Specifically inhibit LH
Anterior Pituitary
Follicle Stimulating
Hormone (FSH)
 Sertoli Cells
Luteinizing
Hormone (LH)
 Interstitial Cells
Inhibin
Androgen Binding
Protein (ABP)
Testosterone
 Spermatogenic cells
Testosterone
Spermatogenesis
Hormonal Control of testicular cells
 Hypothalamus secretes gonadotropin releasing hormone
(GnRH)
 Anterior pituitary secretes FSH and LH
 FSH causes Sertoli cells to secrete:

Androgen Binding protein (ABP)

Inhibin
 LH causes interstitial cells to secrete testosterone
 ABP binds testosterone  its half-life
spermatogenesis
 stimulate
 Control of testicular function:
by Negative FB by
1.  testosterone (on (hypothalamus & ant pituitary;
against LH)
2. Inhibin (on anterior pituitary against FSH)
Sortoli cells
Histology
 Large pyramidal
 Non motile
 Non proliferating
 Tubular cells
Site
line the seminiferous tubules
Function of Sertoli cells
1. Supportive
1. Provide mechanical support for the growing gametes.
2. Spermiogenesis
 Means: Convert spermatids to spermatozoa
3. Spermiation
 Means: release of sperms from Sertoli cells to lumen
of seminiferous tubules
2. Provide nutrition support for growing gametes (high
content of glycogen).
 Mechanism: by removal of excess cytoplasm.
 Control: under the effect of LH.
Function of Sertoli cells
4. Secretory
 Secretion of fluid, rich in K+ , HCO3-,
 Essential subs for maturation of sperms.
Sertoli cells synthesize and secrete the following (under
the effect of FSH):
1. Inhibin
Hormone  ---- FSH
secretion
2. Estradiol from androgenic precursors.
3. Mullerian duct-inhibiting factor  preventing
differentiation of the female internal sex organs in
the male fetus.
4. Androgen-Binding Protein (ABP)  binds testosterone
  its half-life
5. Blood-testis barrier:
 Is a memb. formed by tight junctions between the bases of Sertoli cells.
 It has two main functions:
1. It prevents harmful subs. in the bl. from reaching seminiferous lumen.
2. It keeps immunogenic germ cells in the seminiferous tubules from
entering systemic circulation.
6. They Synthesize and secrete H-Y antigen:
differentiate as testes.
 gonadal cells to
B) Leydig Cells (interstitial cells Leydig)
Site
Located between seminiferous tubules (20% of testicular mass).
Time of appearance
Function
They appear at 7-9th week of pregnancy.
They secrete androgens:
1. In the fetal life under effect of human chorionic
gonadotropin (HCG) secreted by the placenta.
2. At puberty under effect of pituitary
gonadotropins).
C) The Spermatogenic cells
The spermatogonia are nonmotile stem cells that
divide during the process of spermatogenesis to
form mature sperms
Spermatogenesis
Def.
Process of formation of spermatozoa from primitive
germ cells.
Time
Starts at average of 13 year throughout whole life
but ing markedly in old age (Andropause)
Site
Seminiferous tubules.
Duration
Needs 74 days (+ 12-21 days for transport of sperms
into the ejaculatory ducts).
Maturation
of Sperms
Occurs in epididymis (needs 18h to 10 days).
Storage of
Sperms
Occurs in the vas deferens in suppressed inactive
state by multiple inhibitory factors.
Factors
affecting
1.
2.
3.
4.
Hormonal (Hypothamamic, testosterone, & others)
Temperature
Dietary
Extrinsic
1. Hormonal Factors
a) Hypothalamic-hypophysial-testicular Axis
At puberty  ++ hypothalamic LHRH  ++
pituitary gonadotropins; FSH and LH.
i) Function of FSH:
1. It maintains the gametogenic functions of
the testes.
2. Stimulate Growth and secretory functions of
Sertoli cells.
ii) Function of LH:
Stimulate Leydig cells  testosterone  ++
spermatogenesis.
b) Testosterone:
Stimulate growth & division of spermatogenic
cells.
Needed in high conc w is maintained by:
1. Lipid solubility of the hormone.
2. Presence of Androgen-Binding Protein (from
Sertoli cells).
3. Counter current exchange: exchange of
testosterone from systemic veins
into
spermatic arteries w runs parallel but in
opposite direction to each other).
Counter current exchange
Note
Counter current system
Counter current exchanger
1. Thermoregulation (testes)
2. Testosterone (testes)
3. Thermoregulation (skin)
4. Vasa recta in kidney
Multiplier system:
kidney
Systemic vein
Spermatic
artery
Systemic vein
c) Other Hormones:
1. Inhibin: ---FSH secretion by a direct effect
on ant. pituitary.
2. Activins:
are
formed
from
precursors and ++ FSH secretion.
inhibin
3. Growth h: stimulates early division of
spermatogonia.
4. Thyroid h:  essential for
reaction of spermatogenesis.
metabolic
2. Temperature
The optimum temp. for spermatogenesis is 35°C
(i.e.< body temp.) provided by:
1. Site of the testes: in the scrotum outside
abdominal cavity.
2. Scrotal skin is thin, rich in sweat glands and
with little subcutanous fat.
3. Counter current system (heat exchange
between spermatic art. and veins).
4. Dartos ms  buffer (contracts in cold and
relaxes in hot weather).
Counter current exchange
Systemic vein
Spermatic
artery
Systemic vein
3. Dietary factors
1. Starvation   gonadotropin sec
2. Vit. A def.  keratinization & atrophy of
spermatogenic epith.
3. Vit. C deficiency  testosterone synthesis
4. Extrinsic factors
Mostly inhibit spermatogenesis:
Irradiation, Hypoxia and toxins , Certain
infections e.g. mumps destroy seminiferous
tubules.
We got too much…..please GOD make
him finish…….
Hormones secreted by the testis
a) Testosterone
 Major hormone produced by the Leydig cells
 More than 98% of it is bound to plasma proteins & 2%
unbound.
b) Dihydrotestosterone
 Only 20% of dihydrotestosterone is synthesized in testis.
 80% from the peripheral conversion of testosterone.
 Dihydrotestosterone is 2 times active than testosterone.
c) Androstenedione:
 Important steroid precursor for blood estrogens in men.
is
Physiological function of testosterone
During fetal life
Differentiation
Testicular
descend
After birth
Sexual
function
Metabolic
function
Physiologic Effects of Testosterone
A) During the
Fetal Life
1- Differentiation & development of 2ry sex organs:
Leydig cells of testes secrete testosterone at 79th week of gestation  ++ Wolffian duct 
internal genitalia in male.
2- It helps descend of testes from abd. cavity into
scrotum during the last 2 to 3 months of pregnancy.
B) After Birth
(1) Sexual
functions
1- 1ry sex organ  Spermatogenesis
2. 2ry sex organs Growth & enlargement.
3. Control of gonadotropin secretion (-ve FB)
4. Development of male sex characters:
a) Hair:
 Hair especially in face, on chest, axilla and
around anus.
 Pubic hair is triangular in appearance with apex
towards umbilicus.
 The hair disappears from ant. part of scalp
“temporal recession”.
2ry sex characters
b) Voice:
Deep & low pitched ( thickness of vocal cords).
c) Skin:
is thickened with acne formation. ‫حب الشباب‬
d) Body conformation
Shoulders broaden and ms enlarge.
e) Behavioural changes
 sexual desire & males become aggressive.
(2)
Metabolic
Effects
1- Protein-anabolic effect which :
  Ms bulk (50%  in ms mass.
  Bone growth with deposition of Ca2+ and
finally closure of epiphysis.
  Thickness of the skin and vocal cords.
  BMR by 5-10%.
2- Increased RBCs count:
3- Effect on water and electrolytes:
 Moderate Na+, K+, Ca2+,& water retention.
  The size of the kidneys.
Mechanism of Erection
Mechanism of Erection
 The penis consists of erectile tissue made up
of three columns or cords of
vascular spaces
spongelike
 Erection is accomplished by engorgement of
the penis with blood (vasocongestion).
 In the absence of sexual excitation, the
erectile tissues contain little blood,
because their arterioles are constricted.
the penis remains small and flaccid.
 During sexual arousal, these arterioles
reflexly dilate and the erectile tissue fills
with blood, causing the penis to enlarge.
 The veins that drain the erectile tissue are
mechanically compressed  reducing venous
outflow  more vasocongestion.
 Erection is achieved through Erection Reflex
 Parasymp
plays the most important
through its strong VD on the arterioles
role
 The chemical mediator is nitric oxide (NO) that
acts through generation of cGMP
 cGMP
(PDE5)
is inactivated by phosphodiesterase 5
 Sildenafil (Viagra) inhibits PDE5  cGMP 
time of erection (but can’t initiate erection as
it can't generate nitric oxide (NO)
Mechanism of Erection
Release of NO within the penile tissue
Generation of c GMP
Relaxation of smooth of bl vs
Dilatation arterioles & arteries
Expanding of sinusoids in corpora cavernosa
Compression of subtunical venular plexuses
Increasing of intracavernous pressure
Increased resistance to outflow from penis
MALE SEXUAL PERFORMANCE
Erectile dysfunction or Impotence:
Failure to achieve or maintain an erection suitable for sexual intercourse.
Affect 50% of men between 40 and 70 years old. May be due to:
1. Psychological factors.
2. Physical factors.
A. Nerve damage
B. Medication that interfere with autonomic function
C. Problem with blood flow to the penis.
Sildenafil (Vigra): prescribed to treat erectile dysfunction. It does not
produce an erection but it amplifies and prolongs an erectile response
triggered by usual means of stimulation.
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ABNORMALITIES OF TESTICULAR
FUNCTION
1. Cryptorchidism:
descent of testes is incomplete, testes remain in the abdomen. Occurs in
neonatal life.
1. Bilateral: Impaired Testosterone secretion and spermatogenesis.
2. Unilateral :Normal Testosterone and impaired spermatogenesis.
2. Male hypogonadism:
Clinical picture depends on whether testicular deficiency develops before or
after puberty.
causes:
– Testicular disease (Hypergonadotrophic Hypogonadism)
– Disorder of hypothalamus or pituitary (Hypogonadotrophic
Hypogonadism)
3. Androgen secreting tumors :
Leydig cell tumors (a rare condition) leads to precocious pseudopuberty in
prepubertal boys.
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REFERENCES
 Human physiology, Lauralee Sherwood, seventh
edition.
 Text book physiology by Guyton &Hall,11th
edition.
 Text book of physiology by Linda .s Costanzo,
third edition.
 Physiology by Berne and Levy, sixth edition.
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Thanks a lot my friend ………
Thank
You