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Expanding Treatment Options for Erectile Dysfunction

  • Authors: Hartmut Porst, MD
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Target Audience and Goal Statement

This activity is intended for urologists, primary-care physicians, and internists.

The central goals of this educational activity are to enhance recognition of, and care for, erectile dysfunction (ED) by exploring the epidemiology of this underrecognized condition, discussing interview and other diagnostic techniques, and considering the evidence supporting distinct treatment approaches.

Upon completion of this self-study activity, participants will be able to:

  1. Appreciate the true dimensions of ED and the needs of many patients and their partners more accurately.
  2. Enumerate risk factors for the condition.
  3. Discuss current first-line diagnostic assessments for ED, including a focused physical examination and three types of history: medical, sexual, and psychosocial.
  4. Delineate the biochemical cascade underlying physiologic erection.
  5. Discuss the effects of first-, second-, and third-line treatment modalities on ED.


  • Hartmut Porst, MD

    Professor of Urology, Medical University of Bonn, Germany.


    Disclosure: Hartmut Porst, MD, has disclosed that he serves as an advisor or consultant for Bayer, Pfizer, and Merck Germany. He serves an investigator for Lilly ICOS LLC, Takeda, Abbott, and Merck Germany. In this activity, Dr. Porst discusses the investigational product Tadalafil to treat erectile dysfunction.

Accreditation Statements

    For Physicians

  • Medical Education Collaborative, a nonprofit education organization, is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

    Medical Education Collaborative designates this educational activity for a maximum of 1.5 hours in Category 1 credit towards the AMA Physician's Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity.

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Expanding Treatment Options for Erectile Dysfunction: PDEs and PDE Inhibition


PDEs and PDE Inhibition

The 3',5'-cyclic nucleotide PDEs are key regulators of intracellular cGMP and cAMP activity and, hence, relaxation of corporal smooth muscle.[13,14] Known to occur in at least 11 isoforms and isoenzymes, these enzymes are distributed in nearly all body tissues, with clearly distinct concentrations, depending on the respective functions of the tissues. The PDEs are responsible for enzymatic degradation of the biologically active cGMP and cAMP to the biological inactive molecules GMP and AMP.

Within the corpus cavernosum and other tissues, multiple PDE isoforms are expressed as products of either different genes or the same gene produced by alternative splicing. Messenger RNA for at least 13 PDE5 isoforms and isoenzymes were identified within the human corpus cavernosum,[15] a finding that was indicative of the complexity of penile erection physiology.

By inhibiting the degradation of cGMP, PDE5 inhibitors prolong the activity of this cyclic nucleotide second messenger within the cavernous vasculature and smooth musculature, thus potentiating the erectile response. The prototype of this new class of selective PDE5 inhibitors for the treatment of ED was sildenafil. The new selective PDE5 inhibitor tadalafil, which is now under review with the Food and Drug Administration (FDA) and the European Agency for the Evaluation of Medicinal Products, significantly potentiated relaxant responses of human corporal smooth muscle tissues to sodium nitroprusside (Figure 5), acetylcholine, and electrical stimulation. Similar potentiating effects were observed when human penile resistance arteries were exposed to sodium nitroprusside or acetylcholine (Figure 6) in the presence of tadalafil. Consistent with the mechanism of action for PDE5 inhibitors, tadalafil induces no physiologic erection in the absence of sexual stimulation.

  • Figure 5. Relaxant Response of Human Corpus Cavernosum to Sodium Nitroprusside in the Presence of Ta

    Figure 5.

    Relaxant Response of Human Corpus Cavernosum to Sodium Nitroprusside in the Presence of Tadalafil

    (Enlarge Slide)
  • Histological studies indicate that PDE5 is expressed by penile resistance arteries and smooth muscle tissue, and clinical evidence reinforces the central functional role of PDE5 in potentiating NO/cGMP-mediated smooth muscle relaxant effects in the male erectile response. Analogous cases exist in other tissues with intrinsic PDE activity. For instance, milrinone, a PDE3 inhibitor, enhances relaxation of trabecular smooth muscle in the heart but exerts a much less prominent effect within human penile resistance arteries.

    Functional studies have demonstrated that PDE4 is expressed in both penile arteries and muscle tissues, among other widely distributed tissues, and its activity is inhibited by rolipram.[13] On the other hand, cardiac myocytes chiefly express calcium/calmodulin-dependent PDE1; human saphenous veins express PDE1, PDE4, and PDE5; and human mesenteric arteries express PDEs 1 through 5.[15] In animal models, sildenafil selectively augmented cGMP levels in coronary vascular smooth muscle and also potentiated the hypotensive effects of NO donor agents on these tissues.[16]

  • Figure 6. Relaxant Response of Human Penile Resistance Arteries to Acetylcholine in the Presence of

    Figure 6.

    Relaxant Response of Human Penile Resistance Arteries to Acetylcholine in the Presence of Tadalafil

    (Enlarge Slide)