Erection

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Erection

During erection, erectile tissue stiffens by engorging with blood. Although the term erection typically is used to describe sexual arousal of the penis, other tissues, such as the female vagina and clitoris and the nipples of both men and women, are capable of erection.

The male penis is composed of three compartments: one along each side (the corpus cavernosum; plural, cavernosa) and the central compartment (the corpus spongiosum). The corpus spongiosum, which surrounds the urethra, does not experience significant engorgement. The corpora cavernosa are surrounded by the tunica albuginea, a fibrous membrane that resists expansion, causing the penis to engorge and stiffen in as little as ten to fifteen seconds. The corpus spongiosum lacks the tunica and does not stiffen during arousal. The penile glans assumes a dark purplish hue as it becomes engorged but, like the corpus spongiosum, does not stiffen.

Although a range of stimuli may initiate arousal, a spinal reflex is the physical basis of erection. Response to direct tactile stimulation is mediated through the spinal column in the sacral region. Response to non-tactile stimulation (fantasy, memory, visual images, etc.) is triggered by a signal from the brain to a region higher in the spinal cord (the lumbar region), which then transmits impulses to the penis. When those nerve impulses are sent to the penis—regardless of the source of stimulation—arteries carrying blood to the corpora cavernosa dilate, and the penis then becomes erect. Erection normally is preceded by sexual desire, which is regulated partly by androgen-sensitive emotional factors. Although men with androgen deficiency experience fewer and/or less vigorous spontaneous erections, they can continue to have erections in response to erotic stimuli. It generally is recognized that androgen levels within normal limits are necessary for normal sexual desire but not for erection itself.

Erections do not occur solely during waking hours; they are common during rapid eye movement (REM) sleep cycles (typically every ninety minutes during sleep). These are known as nocturnal erections. Although the exact mechanism is unknown, it appears that nocturnal erections are physiologically based, assuming that the male is not experiencing erotic dreams during this regular cycle. Erections can occur in unconscious or comatose men, presumably by the same mechanism. In some males, notably adolescents, the erectile response is tripped readily; relatively benign stimuli such as accidental contact and brief visualization can trigger an erection.

Erection is reversed when the nerve impulses lessen or cease and more blood flows out of the corpora cavernosa than flows into it. Penile circulatory balance is restored, and the penis returns to its normal resting state. Higher brain functions and impulses can interfere and cause a loss of erection; examples include performance anxiety, fear, preoccupation, and lack of desire.

Spinal injuries to the higher lumbar region result in inability to achieve an erection in response to mental processes but do not impair erection from direct stimulation. Injuries in the sacral region often block all erectile responses.

Erectile dysfunction (ED) can be caused by physical or nonphysical (psychological) factors.

Nonphysical causes include psychological issues such as stress, anxiety depression, and fatigue. Negative feelings between partners, including fear, resentment, hostility, and lack of interest, can affect the ability to generate or maintain an erection.

A myriad of physical issues and disorders, such as hypertension, coronary artery disease and other vascular disorders, chronic disease of the lungs and liver, multiple sclerosis, chronic arthritis, diabetes, chronic renal impairment, chronic alcoholism, and drug abuse, can cause ED.

Many prescription and nonprescription medications, such as antidepressants, antihypertensives, antihistamines, tranquilizers, sleeping aids, and pain medications, can cause or contribute to ED. Chronic alcohol or marijuana use can cause both ED and a decrease in sexual drive; by shrinking the small blood vessels in all parts of the body, excessive tobacco smoking can cause decreased blood flow to the penis.

Prescription medications for the treatment of ED act primarily by relaxing the smooth muscles of the penis, allowing greater blood flow for erection. However, those medications cannot be used in combination with any form of nitrate, such as nitroglycerin or illegal nitrate "poppers"; the combination may be fatal.

In women tissues of the vagina and clitoris respond to nerve reflexes during sexual arousal. When a woman is aroused, blood flow to the labia majora and labia minora is increased, the tissues engorge with blood, and the labia flatten and spread open. The clitoris becomes enlarged and stiffens. The upper portion of the vagina expands and retracts the uterus and cervix, forming an enlarged space.

The nipples of both women and men are capable of erection. Muscles surrounding the nipple contract with sexual arousal, local blood vessels become engorged, and the nipples become erect. Nipples also may become erect during breast-feeding, as a result of fear or excitement, and in response to cold temperatures.

see also Erectile Tissue; Penis.

BIBLIOGRAPHY

McConnell, John D., and Jean D. Wilson. 1991. "Alterations in Reproduction and Sexual Function." In Harrison's Principles of Internal Medicine. 12th edition, ed. Kurt J. Isselbacher, Joseph B. Martin, Eugene Braunwald, et al. New York: McGraw-Hill.

Merck Research Laboratories. 1992. "Sexual Dysfunction in the Male." In The Merck Manual of Diagnosis and Therapy. 16th edition, ed. Mark H. Beers, Robert Berkow, Robert M. Bogin, and Andrew J. Fletcher. Rahway, NJ: Merck Research Laboratories.

Rathus, Spencer A., Jeffrey S. Nevid, and Lois Fichner-Rathus. 2005. "Male Sexual Anatomy and Physiology." In Human Sexuality in a World of Diversity. 6th edition, ed. Spencer A. Rathus, Jeffrey S. Nevid, and Lois Fichner-Rathus. Boston: Pearson Allyn and Bacon.

                                        Christine R. Rainey

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