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Hypertension Erectile dysfunction has a high prevalence among patients with both treated and untreated hypertension. Large studies have confirmed that, not only was ED more prevalent in patients with elevated blood pressure than controls, but also that the degree of ED that experienced by patients with hypertension was also more severe in nature than in the general population.

One study highlighted the specific penile vascular effects of hypertension through the use of rat models.
The study found that hypertensive rats demonstrate impairment in endothelial-mediated relaxation of corporal cavernosal strips in response to acetylcholine. This finding suggested that a defect exists in endothelial-dependent reactivity as well as a reduction in nitric oxide in the presence of hypertension.

It is somewhat more difficult to evaluate the exact effect of hypertension on erectile function in humans. Patients are often being treated for their hypertension with medications that are themselves known to cause ED, such as beta blockers and thiazides. It is likely that the ED experienced in hypertensive men is caused by penile vascular arterial changes including atherosclerosis Obesity Obesity, which is an independent risk factor for cardiovascular disease, is also associated with ED. Esposito et al. showed that intervention with the modification of lifestyle behaviors that led to weight loss and decreased cardiac risk also led to the improvement in erectile function.

A decrease in body mass index may reduce the risk of both ED and endothelial dysfunction in obese men.
If obesity is positively associated with endothelial dysfunction and increased serum concentrations of vascular inflammatory makers, with what has been previously aforementioned, it would appear that a common pathway exists – patients suffer from both increased cardiovascular risk and ED per similar physiologic pathways.

In a more recent publication, Esposito et al. stated that obesity increases ED risk by 30–90% compared to controls. The authors again agreed that lifestyle changes aimed at reducing body mass index improves both erectile and endothelial function in men. In addition, they mentioned that Mediterranean-style diet may aid sexual function.

A separate literature review in 2006 was completely dedicated to the topic of the Mediterranean-style diet and its relation to sexual function. They found that sexual function can improve in as little as 2 years through exercise and adoption of the Mediterranean-style diet. Specifically, men consuming more fruits, vegetables, nuts, whole grain, and olive oil as compared with controls were found to have an improved endothelial function score and improved levels of inflammatory markers.

Risk factors for ED have been delineated in large prospective studies, such as Massachusetts Male Aging Study (MMAS), Boston Area Community Health Survey (BACHS), and Health Professionals Follow-up Study (HPFS). The MMAS study reported on males between ages 40 and 70 years and found that erectile function declined precipitously with age. Overall, the study found that 52% of men within this age range suffered from some degree of ED. Diabetes, heart disease, and hypertension increased the risk of ED significantly in this study.

Erectile dysfunction was studied in men aged 45–70 years with a 14-year follow-up in the HPFS. Excluding men who developed prostate cancer, the relative risk (RR) of development of ED as per self-assessment was 1.5 for current smokers and 1.9 for obese men. In contrast, moderate exercise decreased the risk of ED. Interestingly, these risk factors produced greater effect in men 55 years or younger.

The BACHS was created specifically to assess urologic symptoms in a diverse cohort.

• This study found a dose-response effect of tobacco cigarettes on ED, although there was not a significant increase in the odds of developing ED until over 20 pack-years of the habit.
• They also found that low socioeconomic status, independent of other risk factors, including race, was a risk factor for ED.

Erectile Physiology A successful male penile erection requires two processes. Cavernosal artery smooth muscle relaxation and increased venous outflow resistance. In order to sustain an erection one must achieve and maintain a high arterial inflow and a low venous outflow. Cavernosal arterial smooth muscle relaxation is an active process and the initial event of an erection. viagra tablets online

1. Smooth muscle relaxation leads to arterial dilation which results in increased penile blood flow that in turn causes radial and longitudinal cavernosal expansion. This process is mediated by nitric oxide released through stimulation of nonadrenergic, noncholinergic nerves (NANC).

2. Nitric oxide binds to smooth muscle cells stimulating the production of cyclic GMP, which then decreases intracellular calcium and causes relaxation. Cyclic AMP, a second minor messenger, acts in a similar manner to decrease intracellular calcium and causes muscle relaxation.

Venous outflow resistance, in contrast to arterial smooth muscle relaxation, is a passive process. As the cavernosal tissues engorge and expand, they compress the subtunical venous sinuses and cause the outflow resistance necessary to maintain an erection.

Because the brain is intimately involved in the control of erections, a wide variety of psychological factors impact erectile response and may lead to erectile dysfunction (ED).

This chapter reviews the assessment of psychological factors in ED, the immediate and underlying psychological conditions involved, and the development of ED over time. Outcome research on psychological treatments for ED is also reviewed. The goal of the chapter is to help health care providers to conduct a comprehensive evaluation of ED that is sensitive to psychological factors.

A comprehensive understanding of erectile dysfunction (ED) must incorporate both the physical and the psychological aspects of erectile response. An erection is best characterized as a psychophysiological phenomenon that depends on a complex interplay of biological and psychological factors. Impairment in any of these aspects may lead to erectile dysfunction. The focus of this chapter is on the assessment of psychological factors that contribute to erection difficulties. The evidence regarding the outcome of psychological treatments and the integration of medical and psychological treatments are also reviewed.

The definition of psychological factors to be used here encompasses a variety of mental aspects of sexuality.

1. First are the behavioral aspects, which primarily involve who does what to whom in the sexual encounter.
2. Second are the emotional aspects of the sexual response, that is, feelings during sex, as well as the emotional needs associated with sex.
3. Third are the cognitive aspects of sexual response, which include knowledge, beliefs, and attitudes about sexuality.
4. Fourth are the interpersonal aspects, i.e., the couple’s interaction and the quality of the relationship, both sexual and emotional.
5. Fifth are the cultural aspects of sexuality, which entail the expectations and norms that shape sexual behavior.

It is also important to note that, while most of these aspects of sexuality are either observable or may be described by the patient, much of what is referred to as psychological is either unconscious or inaccessible to the individual himself.

Oxytocin Proerectile projections from the supraoptic area of the hypothalamus and the PVN travel to the spinal centers for erection and oxytocin has been shown to be a key neurotransmitter in these neurons. In lab animals, intracerebroventricular or intrathecal injection of oxytocin antagonists blocks the induction of erection that is seen with intrathecal oxytocin injection. Additionally, antagonist injection into the lateral ventricles leads to a dose dependant reduction in noncontact erections.

This has led to the belief that oxytocin plays a role in facilitating nonreflexive erections. Dopamine Dopaminergic neurons project to the MPOA and PVN  and also have been discovered to travel from the caudal hypothalamus to the lumbosacral spinal cord.

Dopamine is thought to participate in central regulation of the autonomic and somatic penile reflexes. The dopamine receptor agonist, apomorphine, induces penile erection in rats when administered systemically. Additionally, apomorphine injection into the MPOA facilitated erections while dopaminergic antagonist injection into the MPOA decreased penile reflexes.

In the PVN, dopaminergic neurons appear to stimulate oxytocinergic neurons, which then more directly account for the erectile response. This is supported by the prevention of apomorphine-induced erections in the presence of oxytocin receptor antagonists.

Serotonin In experimental animal models, bulbospinal neurons containing serotonin (5-HT) project to the lumbar spinal cord. Serotonergic fibers have been demonstrated in close proximity to retrogradely labeled sacral preganglionic neurons.

One study showed 5-HT in general had an inhibitory effect on male sexual behavior. However, there have been conflicting reports with another study showing that the stimulation of 5-HT2c receptors mediated the erectile response. Thus, the full function of 5-HT in erectile function has not been fully elucidated. It appears to serve various functions likely acting as a major modulator of the central control of erection.