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NAME : UGORJI OLUOMACHI GRACE
MATRIC NUMBER: 13/MHSO3/016
DEPARTMENT : ANATOMY
COURSE: REPRODUCTIVE PHYSIOLOGY
PHYSIOLOGY OF COITUS
INTRODUCTION:
Coitus is the sexual union between a male and female involving
insertion of penis into the vagina in which there is excitement until
orgasm and ejaculation occur.
Considered from this viewpoint, the process of coitus with the
subsequent climax may be profitably studied in both sexes in human
which throw light on human processes of conception. The following are
physiological criteria for orgasm:
(1) Changes in blood pressure, respiratory pattern and heart rate.
(2) Changes in muscular tension (including vaginal and uterine
contraction
(3) Hormonal changes.
(4) Emission of sound
-Blood pressure, heart rate and diastolic pressure increases slightly for
a short time but recovers to the baseline after sexual activity.
Hormones such as oxytocin, prolactin and endorphins are released
during sexual activity
Vagina flatulence occurs doing coitus, this is due to emission of air from
the vagina
PHYSIOLOGY OF COITUS IN MALE
Erection results from tactile stimulation the penis and adjacent
perineum. The reflex involves the internal pudendal nerves (afferent)
and the parasympathetic outflow from (efferent). Psychogenic stimuli
(e.g. visual cues) can also cause erection so there is descending control.
Erection is caused by relaxation of the smooth muscle of the dorsal
artery and the arteries to the corpus cavernosum. The arteries dilate,
allowing an inflow of blood. Arterio-venous shunts are closed to
prevent drainage and the SM of the cavernosum relaxes, decreasing
resistance to the increase in blood volume there. Venous ‘bleed’ valves
close (and the veins are compressed by the increased pressure) Low
volume, low pressure. The corpus spongiosum does not increase in
turgor as much as the c.c., so compression of the urethra is avoided.
Signaling pathways are still not certain. Autonomic NS involves NA and
ACh. Injection of VIP causes erection, but may ultimately end up as a
nitric oxide (NO) signal (enter Viagra).The testes are drawn reflexively
towards the perineum and the dartos muscle contracts the scrotum.
Testicular volume may increase by 50% due to vasocongestion· Further
stimulation leads to emission, in which the contents of the vas
deferens, prostate and seminal vesicles are expelled into the urethra.
This is followed by ejaculation; in which semen is expelled from the
posterior urethra retrograde ejaculation into the bladder is prevented
by contraction of the vesical urethral sphincter. Other changes of sexual
arousal – nipple erection, -HR, -BP, skin rashes immediately prior to
ejaculation, muscle spasms etc.
PHYSIOLOGY OF COITUS IN THE FEMALE
Psychogenic stimulation, stimulation of the vaginal walls and
particularly the clitoris leads to genital changes very similar to the male.
Vasocongestion of genitalia, including clitoral erection. Other effects
are also similar, though time course differs from the male (i.e. longer).
Subjective descriptions of orgasms are very similar in men and women.
Vaginal lubrication is by transudation of fluid through the vaginal wall.
The vagina increases in width and length and the uterus elevates, lifting
the cervical os to cause tenting of the vagina. At orgasm, vaginal and
uterine contractions occur. The cervix may be actively dipped into the
pool of semen by these contractions. Behavioral differences in sexual
excitability probably reflect differences in reproductive strategy.
Orgasm following coitus occurs in 100% of normal men but surveys
suggest 30-50 percent women.
PHYSIOLOGY OF ERECTION
The human penis is composed of the paired dorsal corpora cavernosa
and the ventral corpus spongiosum each of which is encased within a
fibrous sheath, the tunica albuginea, and then all of which are enclosed
within Buck’s fascia, Colles’ fascia, and the skin. The spongiosum
contains the urethra and is contiguous with the glans distally. The
arterial supply to the penis is from the four terminal branches of the
paired penile arteries, which are the branches of the internal pudendal
arteries. The external iliac, obturator, vesical, and femoral arteries
provide accessory arterial supply to the penile artery in some cases.
Venous outflow originates from postcavernous venules that coalesce to
form emissary veins. These veins empty into the cavernous vein, the
deep dorsal vein, and the superficial dorsal vein depending on their
origin within the penis. Efferent innervation is from parasympathetic,
sympathetic, and somatic sources. Somatosensory afferents course
from the penis to central sites. The maintenance of penile flaccidity and
the erectile response are controlled via intercommunicating supraspinal
and spinal reflex pathways. During the flaccid state, anti-erectile neural
input, primarily via sympathetic efferents, acts to limit blood flow to
the penis to a quantity sufficient to meet physiologic needs but
insufficient for erection. Following either physical or psychological
Sexual stimulation pro erectile neural signals are sent to the penis
primarily via parasympathetic tracts. This input initiates the erectile
response via neurotransmitter release onto postsynaptic smooth
muscle cells within the corporal bodies. NitricOxide (NO) is the main
pro erectile neurotransmitter. The resultant molecular cascade leads to
a decrease in intracellular Ca2+ and arteriolar smooth muscle
relaxation. This relaxation allows for increased blood flow and
subsequent corporal engorgement with increasing penile rigidity. As
the corpora become engorged, the emissary veins are compressed by
within the tunica albuginea limiting venous outflow. The increased
arterial inflow and limited venous outflow increases intracorporal
pressure and leads to erection. As pro erectile input ceases, the
secondary molecular messenger cGMP is hydrolyzed allowing for a rise
intracellular Ca2+, subsequent smooth muscle contraction, decreased
penile blood flow and are turn to flaccid state physiology.