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How Does High Blood Pressure Cause Erectile Dysfunction?


Updated June 18, 2014

Question: How Does High Blood Pressure Cause Erectile Dysfunction?

While nobody knows exactly how high blood pressure is linked to erectile dysfunction, there are several theories that attempt to explain the process. While these theories may seem very different, they are actually all very closely related. Each one is supported by a large amount of clinical and scientific evidence, meaning that the ultimate answer is probably that the cause is a combination of all of these factors below.

High Blood Pressure Causes Blood Vessel Damage

High pressure within blood vessels is known to cause reactionary changes to the physical structure of the blood vessels themselves. For example, it is well known that high blood pressure can cause damage to the small arterioles that feed the kidneys, leading to an impaired ability of the kidney's to filter blood. A similar action may be at work in erectile dysfunction. This theory suggests that high artery pressure in the small vessels of the penis causes microscopic tears to the vessel walls. In the process of repairing these tears, the arteries become thicker and less able to supply needed blood to the spongy, erectile tissues of the penis.

High Blood Pressure Causes Hormone Changes that Lead to Erection Problems

Special tissues in the body are responsible for producing chemicals called hormones, which regulate everything from weight gain and bone growth to sexual drive and erectile response. One theory of how high blood pressure contributes to erectile dysfunction is that elevated pressure in the circulatory system changes some of the natural hormone production faculties of the body. There is some evidence that shows that men with high blood pressure have lower sperm counts and testosterone levels than men with normal blood pressure, leading to speculation that decreased hormonal response to sexual stimulation may play a role in erectile difficulties these men may experience.

High Blood Pressure Lowers Nitric Oxide Levels

The regulation of blood vessel tone – how wide or narrow the blood vessels are – is a complicated process that employs many chemical and physical mediators. Of the many substances that affect blood vessel tone, nitric oxide is among the most important. Produced by specialized cells in the body, nitric oxide is a powerful agent that makes blood vessels relax, or dilate. Some studies have shown that people with long term hypertension (high blood pressure) may produce less nitric oxide over time, causing a decreased capacity for “on demand” blood vessel relaxation. In these cases, erectile dysfunction may result when the body simply can’t produce enough nitric oxide to sufficiently relax penile blood vessels. As a result, the extra blood required to fill the penis cannot be delivered, leading to erectile dysfunction.

Venous Leak

In order to maintain an erection, blood not only has to be supplied to the penis, it also has to stay there. Some research suggests that men with high blood pressure may have difficulty maintaining an erection because the increased pressure actually forces blood out of the erectile tissues of the penis and into the veins. In this theory, the “push” on the small closing valves of the veins is stronger than the veins’ ability to resist. As a result, the veins are not able to “close” tightly enough to stop blood from passing out of the penis, causing difficulty in maintaining an erection.

No single theory has yet accounted for all of the observed factors present in men with high blood pressure who have erectile dysfunction. Rather than one single theory, the full answer is likely to be some combination of factors related to each of these individual ideas.


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  2. Burnett, AL, Lowenstein, CJ, Bredt, D, et al. Nitric oxide synthase: A physiologic mediator of penile erection. Science 1992; 257:401.
  3. Saenz de Tejada, I, Goldstein, I, Azadzoi, K, et al. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. New England Journal of Medicine 1989; 320:1025.
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