Your choice of blood pressure medications could make a difference in the bedroom (or wherever you like to have sex). Thiazides (diuretics or “water pills”) and beta blockers are the most likely to cause erectile dysfunction (ED), while alpha blockers the least likely. Alpha blockers work by reducing nerve impulses to blood vessels, allowing blood to pass more easily. Ask your doctor whether these or other blood pressure medications are best for you.
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
Crossref | PubMed | Scopus (77) | Google ScholarSee all References Nitroglycerin is a vasodilator that is commonly used as an antianginal agent because of its ability to improve the imbalance between myocardial oxygen supply and demand.65x65Stamler, JS, Loh, E, Roddy, MA, Currie, KE, and Creager, MA. Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans. Circulation. 1994; 89: 2035–2040

Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.
PubMed | Google ScholarSee all References Diabetes was found to play a major role in vasculogenic impotence in a study of 265 patients with ED who underwent color duplex ultrasonography of the cavernosal arteries after intracavernosal injection of prostaglandin E1.13x13Chung, WS, Shim, BS, and Park, YY. Hemodynamic insult by vascular risk factors and pharmacologic erection in men with erectile dysfunction: Doppler sonography study. World J Urol. 2000; 18: 427–430
The medicine causes blood vessels to expand, increasing blood flow in the body and to the penis, thus helping patients to get an erection. Invasive surgeries that involve rods and balloons are also available to patients suffering from ED. While these treatments often come with potential side effects, discomfort and a financial burden, some ED patients may see success with them.
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
In most men, ED is recognised as sharing vascular aetiology with IHD.17 ED and IHD share common risk factors, such as hypertension, hyperlipidaemia, diabetes, obesity, lack of physical exercise, cigarette smoking, poor diet, excess alcohol consumption and psychological stress, including depression.30 Endothelial dysfunction has been implicated as a common mechanism between CAD and ED and it has an important role in the development of atherosclerosis.31

While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.

Core tip: The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, phosphodiesterase-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease with obvious benefits for cardiovascular event prevention.
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
Tribulus terrestris is a dicotyledonous herbal plant of the Zygophyllaceae family, used to increase serum testosterone levels, which has only been shown in animal studies (40). A prospective, randomized, double blind study of 30 men showed that Tribulus terrestris was not more effective than placebo on improving IIEF scores or serum total testosterone (41). Two accounts of hepato-nephrotoxicity have been reported in young men who ingested high doses of this herbal medication (42,43).
Erectile dysfunction (ED) is generally defined as the persistent (at least 6 months) inability to achieve and maintain penile erection sufficient to allow satisfactory sexual performance.1 It is a common condition, and recent studies predict a higher prevalence of ED in the future.2 It is estimated that ED has affected more than 150 million men worldwide and this number will reach approximately 322 million by 2025.2,3 It has affected 30 million men in the US alone.4
The research is based on a Swedish national database of health records that includes all hospitals in Sweden. Researchers analyzed the records of men age 80 years or younger who were hospitalized for a first heart attack between 2007 and 2013. Tracking the men for an average of 3.3 years following this first heart attack, they compared outcomes among those who subsequently filled a prescription for a PDE5 inhibitor or alprostadil to those who did not. Overall just over 7 percent of men were prescribed an erectile dysfunction drug, 92 percent of whom were prescribed a PDE5 inhibitor and 8 percent of whom were prescribed alprostadil.

Surgical implantation of a penile prosthesis, either the inflatable (2- and 3-piece) or the malleable device, is a feasible technique that offers a third-line treatment and a more permanent solution to the problem of erectile dysfunction. Interestingly, prosthesis implantation receives a significantly high satisfaction rate as evidenced by the proportionate scores in sexual satisfaction scales. Mechanical failure and infection are the two major disadvantages of those prosthetic implants however, their great efficacy, safety and satisfaction rate in general render them an attractive solution when conservative treatment fails[70-74].


Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
Usually patients will try less invasive alternatives to treat impotence before opting for surgery. These alternatives may include supplements, herbs, lifestyle changes and even medications. In cases where other treatments do not work to resolve ED, surgery might be a last-resort option. Surgery involves implanting a penile prosthesis. This is a saline-filled silicone device or a malleable device. Although the likelihood of serious side effects is considered to be low, certain risks are associated with surgery to correct erectile dysfunction. These side effects may include: anesthetic risk, device infection, and device malfunction or mechanical failure. Some studies have found that five years following surgery around 10–20 percent of men experience device malfunction and failure. Infection rates are low. Around one percent of men who opt for this type of surgery get an infection.
Branded Viagra can now be bought over the counter in pharmacies, but please check with your GP first if you have a medical condition. It's important to use a reputable pharmacy, as there is a large market in counterfeit drugs for erectile dysfunction, especially over the internet. These contain varying amounts of the active ingredient and sometimes completely different drugs.
The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
Crossref | PubMed | Scopus (174) | Google ScholarSee all References This study concluded that patients who have stable coronary artery disease who can exercise to 4.5 metabolic equivalents (METs) with a negative or mildly positive stress test and without angina or hypotension can safely take sildenafil. Physicians who prescribe sildenafil should counsel their patients that, if they have chest pain or other cardiac symptoms with sexual intercourse, they should not take nitrates and should immediately call their physician.66x66Jackson, G. Sexual intercourse and stable angina pectoris. Am J Cardiol. 2000; 86: 35F–37F
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.
Several other facts support the close relationship between sexual dysfunction and CV disease. Endothelial dysfunction mediated by decreased nitric-oxide bioavailability as well as atherosclerotic lesions constitute a common pathophysiologic substrate affecting both CV disease and erectile dysfunction, a disease considered to be primarily of vascular origin[76,80-82]. Several traditional CV risk factors (diabetes mellitus, hypertension, dyslipidemia, and smoking) are frequently found in individuals with erectile dysfunction, conferring a detrimental cardiovascular burden to them. More interestingly, the increased cardiovascular risk observed in those patients is independent of the aforementioned CV risk factors[81-88].

The research is based on a Swedish national database of health records that includes all hospitals in Sweden. Researchers analyzed the records of men age 80 years or younger who were hospitalized for a first heart attack between 2007 and 2013. Tracking the men for an average of 3.3 years following this first heart attack, they compared outcomes among those who subsequently filled a prescription for a PDE5 inhibitor or alprostadil to those who did not. Overall just over 7 percent of men were prescribed an erectile dysfunction drug, 92 percent of whom were prescribed a PDE5 inhibitor and 8 percent of whom were prescribed alprostadil.


Montorsi P,  Ravagnani PM,  Galli S,  Rotatori F,  Veglia F,  Briganti A,  Salonia A,  Dehò F,  Rigatti P,  Montorsi F,  Fiorentini C. Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial, Eur Heart J , 2006, vol. 27 (pg. 2632-2639)https://doi.org/10.1093/eurheartj/ehl142

Crossref | PubMed | Scopus (53) | Google ScholarSee all References A study of 24 patients with ED and untreated essential hypertension showed decreased levels of free and total serum testosterone compared with normal controls.31x31Hughes, GS, Mathur, RS, and Margolius, HS. Sex steroid hormones are altered in essential hypertension. J Hypertens. 1989; 7: 181–187
Crossref | PubMed | Scopus (335) | Google ScholarSee all References Glycemia, as measured by glycosylated hemoglobin, also has been associated with the risk of developing ED in diabetic patients.21x21Klein, R, Klein, BE, Lee, KE, Moss, SE, and Cruickshanks, KJ. Prevalence of self-reported erectile dysfunction in people with long-term IDDM. Diabetes Care. 1996; 19: 135–141
The truth is medication or psychosexual counselling are the first treatments a doctor will suggest because they’ve been proven to work. If a doctor has approved a medication for you then it’s safe. If you would still like to see if herbal supplements work for you, then there is a list below of supplements thought to work for erectile dysfunction. Just before you invest your money in them, remember they aren’t proven to work:
Co-authors Stacy Mandras, M.D., Patricia Uber, Pharm. D., and Mandeep Mehra, M.D., conducted systematic independent literature searches using the MEDLINE database and examined a broad range of medical research that focused on chronic heart failure, sexual activity and sexual dysfunction. This literature included data from patient surveys and clinical trials.
The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58

In years past, before nitric oxide and its role in the erectile response was appreciated, testosterone was used to treat sexual dysfunction in men. It proved a partial success as a standalone therapy, resulting in improved erectile potency in 40–60% of men with low-to-normal testosterone levels. The likelihood of success increased, however, if starting testosterone levels were low (usually defined as below 300 ng/dL), in which case improved erections were experienced by as many as 65% of men, compared with 16.7% receiving placebo; topical testosterone preparations were also noted to be superior to oral replacement or injections.21 These findings were confirmed by another study that showed testosterone produced modest improvements in erectile function and libido in men with low-to-normal testosterone levels.22


Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil is taken orally 1 hour before anticipated sexual intercourse and enhances the normal response to sexual stimulation; however, it has no effect on erections in the absence of stimulation.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N

The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
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