Medicationinduced ED is estimated to occur in 25% of men seen in general medical outpatient clinics. The adverse effects related to drug therapy are additive, especially in older men. In this section, we review the existing literature on this subject. It is important to remember that virtually all data with few exceptions are largely subjective reports based on empiric observation, case series, physician and patient surveys, and pre- and postmarketing drug trials. With all of the unvalidated information that exists regarding this subject, it is especially important for physicians to be aware of the disease process being treated and give strong consideration to whether or not the disease pathophysiology itself is contributing to the sexual dysfunction. In addition, physicians should pay particular attention to the presence of other risk factors for ED (i.e., the patient’s psychosocial status) which exist outside of the disease being treated and the drug in question. The final section of this chapter addresses management strategies for the treatment of druginduced ED.
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The most frequent organic cause of ED is a disturbance of blood flow to and from the penis.
Atherosclerotic or traumatic arterial disease can decrease flow to the lacunar spaces, resulting in decreased rigidity and an increased time to full erection. In theory, any agent that decreases systemic pressure, subsequently altering the hemodynamics of pelvic blood flow, can potentiate ED. Thus, it is not surprising that sexual dysfunction has been associated with nearly all available classes of hypertensive medication. These agents have been strongly correlated with new onset ED.
While hypertension alone is considered a risk factor for ED, a population based prospective study of over 1,000 randomly selected men in the Massachusetts Male Aging Study (MMAS), identified select antihypertensive treatments (specifically thiazide diuretics, spironolactone, b-blockers, methyldopa, and clonidine), and not the condition itself, as an independent risk factor. However, logistic regression analyses with the adjustment for comorbidities and health behaviors attenuated these associations, finding that only nonthiazide diuretics and benzodiazepines were associated with ED to statistical significance. Studies like these make it difficult to interpret the previous literature surrounding antihypertensiveinduced ED.
Among the antihypertensive agents, the b-blockers have been one of the most commonly implicated classes. The prevalence of b-blocker-induced sexual dysfunction has been reported to be anywhere from 5 to 43%. ED has been reported with higher doses of propranolol as well as with other, newer b-blockers as well. The proposed pathophysiology is via decreased corporal blood flow, suppression of CNS sympathetic outflow and in the case of non-specific blockers, inhibition of b2-mediated peripheral vasodilatation leading to insufficient relaxation of the corpora.
Thiazide diuretics are some of the most commonly used antihypertensives. This class is also commonly implicated as eliciting ED. The incidence of thiazide diureticinduced ED has been reported to be anywhere from 4 and 32%. Calcium channel blockers, angiotensinconverting enzyme inhibitors and vasodilators such as hydralazine are other antihypertensive agents linked to druginduced ED. While the mechanism of action is not completely understood, it has been hypothesized that these drugs act directly at the corporal level (for instance, calcium channel blockers) or indirectly by reducing pelvic blood pressure, which is important in the development of penile rigidity. Buy cialis Australia – cheap ed solutions online.
Druginduced ED is not limited to difficulties initiating and maintaining erections. Certain drugs have been reported to induce an absence of ejaculation. Some a-blockers, tamsulosin and silodosin, have been associated with this phenomenon, purportedly through relaxation of the seminal vesicles. While a-blockers have historically been used for hypertension, the practicing urologist is often more familiar with the use of this class of drugs in the treatment of benign prostatic hyperplasia (BPH). Epidemi ologic evidence suggests that ED and BPH are conditions that often arise together. Because preliminary clinical data suggests that the addition of an a1blocker to a PDE5 inhibitor can actually attenuate ED, multiple groups have investigated the effects of concomitant application of various a1blocker and PDE5 inhibitor combinations on human and animal cavernosal tissue as compared to each drug alone. In vitro studies on human tissue demonstrate that the combination of these two drugs exert an additive relaxant effect on cavernosal smooth muscle. In vivo models in the rat suggest that a1blockers can actually increase NO synthesis, alter sympathetic tone and augment blood flow in penile tissue when bladder-outlet obstruction and ED are present.
