Diabetes doubles or even triples the chance that you’ll have erectile dysfunction (ED) and that you could develop it a decade earlier than other men. In fact, the two conditions are so closely linked that some experts believe that for men younger than 45, impotence, or ED, could be an early warning sign of diabetes. The good news is that diabetes treatment, especially if you identify type 2 diabetes early, can also ease ED.
Causes of ED may be of primary developmental origin or secondary. Lack of sex hormone in the early developmental stage of male children is the major cause of primary ED. The secondary cause of ED involves arteriosclerosis, diabetes or psychogenic disturbances. Other secondary factors may include hypertension, hyperlipidaemia, obesity and tobacco use. The primary causes of ED are beyond the scope of this review; we will not be discussing the neurovascular mechanisms pertaining to ED and will focus on the relationship between IHD and ED.
Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28

The 12-week study of 164 men, all with hypertension, was divided into 2 groups of 82, one group with sexual dysfunction, the other group reported normal sexual functioning. Both groups took losartan in dosages of 50 to 100 milligrams daily for the 12 weeks of the study. In the group of men with sexual dysfunction, 88 percent reported improvement in at least one area of sexual function and 73.7% reported an improved quality of life.
Diuretics: Diuretics are also referred to as water pills. They can make the flow of blood to your penis less intense. This makes getting an erection difficult. Diuretics are also known to lower zinc levels, which can decrease the amount of testosterone your body makes. In turn, this can decrease your sex drive. It may also affect your muscle contraction.
Feeling fatigued, very stressed, depressed or dealing with another mood-related issue that can lower libido. Sources of stress and diminished quality of life — such as “deteriorating economic position,” unhappiness with one’s job or other aspects that lower emotional health — are believed to be major causes for sexual dysfunction in both men and women

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].

Whereas lifestyle modification is a reasonable initial step when approaching a hypertensive patient with sexual dysfunction, finding the appropriate antihypertensive treatment is usually the next “complicated” move to care for. Several observational and clinical studieshave consistently associated antihypertensive medication with sexual dysfunction[20]. Whether one class of antihypertensive agents is associated exclusively or more with erectile dysfunction compared to another, however, is a difficult puzzle to solve as there are many other factors (comorbid conditions, concomitant medications, personal characteristics) to be taken into account at the same time. In addition, erectile dysfunction has never been studied as the primary end-point before and as a result a definite causative relationship between antihypertensive medication and sexual dysfunction has never been proven.
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References, 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
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
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

In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).
For those patients who cannot take erectile dysfunction medications, the authors counsel that an exercise training regimen may be an appropriate substitute therapy to enhance sexual function and quality of life. The authors stress that clinicians should focus on the sexual activity history of chronic heart failure patients and not ignore it, since addressing this element can substantially improve their quality of life.
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