The development of an erection is a complex event involving integration of psychologic, neurologic, endocrine, vascular, and local anatomic systems. Positron emission tomography scanning studies have suggested that sexual arousal is activated in higher cortical centers that then stimulate the medial preoptic and paraventricular nuclei of the hypothalamus.5 These signals ultimately descend through a complex neural network involving the parasympathetic nervous system and eventually activate parasympathetic nerves in the sacral area (S2 to S4).

The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[105][106] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[107][108][109]
Late onset hypogonadism reflects a particular pathophysiology and it may not be appropriate to extrapolate results from studies concerning the effects of testosterone in treating hypogonadism of other etiology to aging males. For this reason, the age of men treated in clinical trials is certainly relevant. Other important factors include patient comorbidities and the preparation and route of testosterone replacement used in the study, which can affect the production of estrogen and dihydrotestosterone, testosterone’s active metabolites
Having learned a great deal more about erectile dysfunction including its risk factors and causes, you should be equipped to assess your own erectile function. If you have experienced erectile issues or you have some of the risk factors mentioned above, it may be worth making a trip to your doctor’s office. If you choose to seek help, give your doctor as much information as you can about your symptoms including their frequency and severity as well as the onset. With your doctor’s help, you can determine the best course of treatment to restore sexual function.
Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls. [39]  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.
Begot, I., Peixoto, T. C. A., Gonzaga, L. R. A., Bolzan, D. W., Papa, V., Carvalho, A. C. C., ... & Guizilini, S. (2015, March 1). A Home-Based Walking Program Improves Erectile Dysfunction in Men With an Acute Myocardial Infarction. The American Journal of Cardiology, 115(5), 5741-575. Retrieved from
Due to the risk of hypotension, caution should be used in patients using alpha blockers for prostate hyperplasia and patients using other antihypertensive medications and alpha blockers, which should not be co-administered with PDE5 inhibitors. In patients who take 50 mg of sildenafil or more and use alpha blockers, sildenafil dosing should be avoided for at least 4 hours after the dose of the alpha blocker. In patients who take 25 mg of sildenafil, use of any alpha blockers is considered safe.
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).

But if a man with sleep apnea is diagnosed with low testosterone alone, taking the supplemental hormone can worsen sleep apnea. That's why it's crucial for men with low testosterone to get a thorough workup by an endocrinologist so underlying conditions that can cause low testosterone, such as sleep apnea or pituitary-gland tumors, don't go undiagnosed, Dr. Goodman says.

Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.

Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.