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.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References In conclusion, sildenafil, when used alone, seems to produce minimal decreases in blood pressure level, which are well tolerated in healthy patients and in those with stable ischemic coronary disease.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C

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


88. Böhm M, Baumhäkel M, Teo K, Sleight P, Probstfield J, Gao P, Mann JF, Diaz R, Dagenais GR, Jennings GL, et al. Erectile dysfunction predicts cardiovascular events in high-risk patients receiving telmisartan, ramipril, or both: The ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (ONTARGET/TRANSCEND) Trials. Circulation. 2010;121:1439–1446. [PubMed]
Second-generation cardioselective beta-blockers (atenolol, metoprolol, bisoprolol, etc.) can also lead to ED. Atenolol was shown to cause significant reduction of sexual activity compared with placebo in a double-blind, parallel-arm study.22 The same study also showed a significant reduction in testosterone levels with atenolol versus valsartan. An open, prospective study of hypertensive men treated with atenolol, metoprolol and bisoprolol for at least 6 months showed high prevalence of ED – approaching 66 % – in these patients.23
"Just because there is evidence doesn't mean it's good evidence," says Andrew McCullough, MD, associate professor of clinical urology at New York University Langone Medical Center in New York City, and one of the original clinical investigators for the ED drug Viagra (sildenafil). "And before men with ED start down the naturopathic route, it's smart to make sure that there isn't some underlying medical condition that needs to be corrected." Moreover, it is estimated that 30 million American men have erectile dysfunction, and 70% of cases are a result of a potentially deadly condition like atherosclerosis, kidney disease, vascular disease, neurological disease, or diabetes. Additionally, ED can also be caused by certain medications, surgical injury, and psychological problems.
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.
Heart disease and erectile dysfunction can be related. In fact, ED and heart disease are considered two signs of the same disease process. The smaller arteries in the penis are affected by atherosclerosis sooner, perhaps three or more years before they cause heart disease symptoms.11 A large international study found that men with ED were more likely to die from heart causes; have a heart attack, stroke or be admitted to the hospital with heart failure than men with no or mild ED.12
A number of drugs are known to cause ED in patients with DM (Table 1). For example, many EDDM patients are on antihypertensive medications. Replacement of thiazides or beta-blockers with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be sufficient to regain erectile ability.5 Furthermore, discontinuation of selective serotonin reuptake inhibitors, if these drugs are not essential for patient well-being, may be therapeutic. Careful monitoring following drug discontinuation will help to determine if ED is due to the medication or other underlying disorders. The benefits of continued drug therapy with these drugs should always be weighed against the likelihood of causing ED and impacting on the patient's QOL.
After adjusting for cardiovascular risk factors including diabetes, heart failure and stroke, those taking PDE5 inhibitors were found to be markedly less likely to die than those taking alprostadil or no erectile dysfunction drugs. Filling more prescriptions for PDE5 inhibitors appeared to be associated with a greater benefit, although Andersson said that trend should be interpreted with caution because the study was not large enough for a definitive dose-response analysis.
Not enough info for you? No problem. Nerd out on erectile dysfunction with these studies and research from the most trusted sources on the interwebs. If you have any questions or you think we missed something important, leave a comment or book a consultation with me or one of these trained professionals and we’ll get you on the way to a healthier manhood.
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.
Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
Crossref | PubMed | Scopus (443) | Google ScholarSee all References Nitroglycerin and other NO donors work through the same NO-cGMP pathway that sildenafil affects, thereby decreasing vascular resistance and blood pressure level.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
*all photos are models and not actual patients.If you are interested in a prescription product, Hims will assist in setting up a visit for you with an independent physician who will evaluate whether or not you are an appropriate candidate for the prescription product and if appropriate, may write you a prescription for the product which you can fill at the pharmacy of your choice.
The mechanisms of action by which antihypertensive medications cause ED are currently unknown. Some investigators have theorized that antihypertensive medications affect erectile function by decreasing blood pressure, which reduces the perfusion pressure needed to maintain sufficient blood flow for erections through atherosclerotic penile arteries.37x37Benet, AE and Melman, A. The epidemiology of erectile dysfunction. Urol Clin North Am. 1995; 22: 699–709
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Early work in this field, performed by Masters and Johnson in 1966, involved evaluation of young patients in a laboratory setting and found that heart rates and systolic blood pressure levels during sexual activity approached levels seen during maximal exercise.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F

Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Coital position has not been shown to play a role in increased cardiovascular risk; similar peak heart rates and blood pressure levels are evident with either the man or the woman in the superior position during intercourse.90x90Nemec, ED, Mansfield, L, and Kennedy, JW. Heart rate and blood pressure responses during sexual activity in normal males. Am Heart J. 1976; 92: 274–277
PubMed | Google ScholarSee all References As with sildenafil, use of nitrate or NO-donor medications is contraindicated while taking tadalafil because of the potential for marked hypotensive interactions.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446

Considering the fact that CV disease presents with higher incidence in patients with erectile dysfunction while at the same time sexual activity by itself poses potential CV risks, the appropriate management of those complex conditions is of utmost importance. Accordingly, the working group of the third Princeton Consensus Conference developed practical guidelines and a simplified algorithm in order to manage sexual dysfunction and sexual activity implementation issues in patients with different levels of CV risk, including hypertensive patients[90].


SOURCES: Jackson, G. The Journal of Sexual Medicine, July 2005; vol 2: pp 513-516. Graham Jackson, MD, cardiologist, Cardiothoracic Centre, St. Thomas' Hospital, London. Richard Stein, MD, professor of clinical medicine, Albert Einstein College of Medicine; director of preventive cardiology, Beth Israel Hospital, New York City; spokesman, American Heart Association. Irwin Goldstein, MD, editor-in-chief, The Journal of Sexual Medicine.
Relation between erectile dysfunction prevalence and type of coronary syndrome (A). Time interval (months) between erectile dysfunction and coronary artery disease symptom onset in chronic coronary syndrome according to the number of vessels involved (B). ACS, acute coronary syndrome; CCS, chronic coronary syndrome, G1: ACS and 1-VD; G2: ACS and 2-,3-VD; G3: CCS. VD, vessel disease; C: the control group with normal coronary angiography. With permission from Montorsi et al.15
Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.
The pathophysiological basis for the predictive ability of ED has been discussed above. It should be emphasized, however, that ED should not only be viewed as a manifestation of obstructive CAD that could be identified by ischaemia revealing tests. Owing to the inflammatory and pro-thrombotic activation of the disease,13 it should also be regarded as an early warning sign of an imminent acute event (mainly acute myocardial infarction)22 due to the rupture of a subclinical plaque, and thus identification of the risk should ideally include plaque vulnerability tests. Finally, an issue that has important clinical implications is by how long the clinical manifestation of ED precedes the clinical manifestation of CAD. According to studies, men with ED and no cardiac symptoms have an increased incidence of experiencing a cardiac event, both acute and chronic, in the ensuing 2–5 years, thus providing a ‘window of opportunity’ for risk reduction management in these patients.2
Abstract | Full Text PDF | PubMed | Scopus (1528) | Google ScholarSee all References After sexual intercourse, this risk increases approximately 2-fold, to 2 chances per million per hour, but only for the 2 hours after intercourse. For low-risk patients with no history of cardiovascular disease and an annual myocardial infarction risk of 1% per year, the risk increases to 1.01% with weekly sexual activity.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
Abstract | Full Text PDF | PubMed | Scopus (29) | Google ScholarSee all References After controlling for diabetes mellitus, tobacco use, and hyperlipidemia, hypertension was not found to be an independent predictor of vasculogenic ED in 440 impotent men as measured by the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.

Crossref | PubMed | Scopus (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
For patients who failed oral medical therapy or unable to tolerate the side effects, intracavernosal injection of vasoactive agents can often provide effective alternative. Various vasoactive agents such as alprostadil, papaverine or phentolamine have been used either as single agent or combination agents to potentiate the NO release and cavernosal smooth muscle vasodilation. However, intracavernosal injection therapy has high attrition rate and can be associated pain especially with alprostadil injection (2). The practice of isolating compounds and understanding its pharmacological attributes before using it as a drug therapy has been a strength of Western medicine.
The authors observe that multiple factors may be involved. In addition to decreased exercise capacity, patients with chronic heart failure have blood vessel and circulation abnormalities that can reduce blood flow into the penis and interfere with the ability to maintain an erection. And erectile dysfunction can be caused or worsened by many of the medications that are commonly prescribed to treat chronic heart failure.

Crossref | PubMed | Google ScholarSee all References In the general population, the estimated relative risk of experiencing a myocardial infarction within 2 hours after sexual intercourse is approximately 2.5 times higher than the baseline infarction risk of that individual, which itself is extremely low8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409


A limitation of the study is that the researchers did not assess the effects of untreated erectile dysfunction, or conversely, the effect of having an active sex life without taking erectile dysfunction drugs. The researchers also were unable to account for socioeconomic status; as a next step, they are planning a larger study that will include more health records and complete information on marital status, educational level and disposable income. They are also pursuing a separate analysis of outcomes from erectile dysfunction drugs in men with Type 1 and Type 2 diabetes.
PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Vision changes are described most frequently as an increased perception of bright lights, a blue-green tinge to observed colors, or blurred vision. Sildenafil has no direct effect on platelet function but potentiates the inhibitory effect of sodium nitroprusside on adenosine diphosphate–induced platelet aggregation ex vivo.56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
If not properly controlled, both type 1 and type 2 diabetes can cause complications due to high blood sugar levels. Over time, these high levels can cause irreversible nerve damage and narrow your blood vessels. While nerve damage may affect the sensitivity of your penis, blood vessel damage can affect the blood flow to your penis and make it more difficult for you to get an erection.
Chronic heart failure often develops after other cardiac problems have damaged or weakened the heart, leaving it too weak or too stiff to fill and pump efficiently. Many underlying heart conditions can lead to heart failure. It can develop quickly after damage caused by a heart attack, or it can develop gradually after years of high blood pressure or coronary artery disease.
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.

Some blood pressure medicines can also cause erectile dysfunction. Thiazide diuretics and beta-blockers are most likely to cause problems, but this is not a common effect of these medicines and will not happen to everyone. If you are taking either of these medicines and are worried about erectile dysfunction, your GP may be able to change your medicines.
In Western medicine approach, health and disease are clearly divided entities. The emphasis is on protection of the individual body from disease or how to replace the body’s lost functions. Antibiotic therapy is used to combat harmful bacteria during infections, exogenous synthetic hormones are used to replace hormone-deficient individuals and artificial prostheses are applied when an organ loses its functions. This is very different from the holistic Eastern approach where the treatment entity is taken as a whole, and the objective is to seek harmony between different bodily systems.
There are a number of reasons a man may not achieve the desired result from an oral erectile dysfunction drug. In some cases, a man may experience drug side effects severe enough to outweigh any potential benefit of taking the drug. Possible side effects of these drugs include headache, facial flushing, nasal congestion, and transient abnormal vision. (In October 2007, the FDA added a warning about sudden hearing loss to the package labels of oral erectile dysfunction drugs. While it’s not absolutely clear that the drugs can cause sudden hearing loss, a number of cases have been reported in men within hours or days of taking one of the drugs.)
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