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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.

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  • 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: Physiology of Penile Erection


Physiology of Penile Erection

With sexual arousal through imaginative, visual, auditory, tactile, olfactory, and other erotic stimuli, nitric oxide (NO) is released by nonadrenergic, noncholinergic (NANC) neurons.[11] Originally termed endothelial-derived relaxing factor, NO is known to be the most important physiologically occurring vasoactive molecule in the entire cardiovascular system. This also applies to corpus cavernosum function, where local smooth muscle relaxation, and in turn erection, is mediated predominantly by NO release.

Dilation of the helicine arterioles and relaxation of the sinusoids lead to engorgement of sinusoidal spaces with blood. Expansion against the tunica albuginea compresses blood-draining subtunical venules, resulting in blockade of cavernous venous outflow. This leads to complete filling of the cavernous sinusoids and subsequently to a considerable increase of the intracavernous pressure. In the phase of full rigidity, intracavernous pressure reaches values considerably higher than systemic (systolic) blood pressure.During male sexual arousal, NO is released either at parasympathetic NANC nerve terminals on the cavernous smooth muscle cell or at parasympathetic cholinergic nerve terminals on the endothelial cell lining of the sinusoids. Through membrane-bound G proteins, NO activates guanylate cyclase, which induces cleavage of guanosine triphosphate to 3',5'-cyclic guanosine monophosphate (3',5'-cGMP).The smooth muscle-relaxing effects of NO are mediated by this second messenger(cGMP). Cyclic GMP activates protein kinase G (PKG), which phosphorylates proteins at the so-called maxi-potassium channels. This results in an outflow of potassium (K+) ions into the extracellular space with subsequent hyperpolarization, with inhibition or blockade of voltage-dependent calcium (Ca++) channels and therefore a decrease in intracellular Ca++ ion concentrations (Figure 4).

  • The intracellular decline in Ca++ ions suppresses the activity of myosin light chain (MLC) kinase and thus increases the intracellular content of dephosphorylated MLC, which enables the smooth muscle cell to relax.[12] It is well established that NO and cGMP are the most important transmitters for onset and maintenance of erection. In physiologic terms, 3',5'-cGMP is permanently broken down to the biologically inactive 5'-GMP by the enzyme PDE5.

    Cyclic adenosine monophosphate (cAMP), a further second messenger in erectile function, plays an inferior role when compared with cGMP. When erection occurs, vasoactive intestinal polypeptide (VIP) is released at parasympathetic NANC nerve terminals, as is similarly the case with NO release. Both NO and VIP are in colocalization at the respective NANC nerve terminals and are released simultaneously with sexual arousal. VIP activates membrane-bound adenylate cyclase, which promotes cleavage of adenosine triphosphate to 3'5'-cAMP. cAMP activates protein kinase A, which phosphorylates proteins adjacent to the maxi-potassium channels, resulting in K+ ion outflow and hyperpolarization. In turn, the same biochemical actions take place as were described for 3'5'-cGMP.

    Apart from these proerectile mechanisms, other biological pathways are important either for inducing or inhibiting erection. In particular, activation of the sympathetic nervous system, which occurs, for example, with performance anxiety, results in inhibition of erection. With increased sympathetic tone, norepinephrine is released at alpha1-adrenoceptors located on the cavernous smooth muscle cell. Norepinephrine activates membrane-bound phospholipase C, which induces cleavage of phosphoinositol diphosphate to inositol triphosphate and diacylglycerol. Both inositol triphosphate and diacylglycerol cause an increase in intracellular Ca++, which in turn activates MLC kinase and leads to an increase in phosphorylated MLC.[12] This enables the smooth muscle cell to contract and thus prevent erection. In addition, endothelial vasoactive compounds, such as endothelin 1, angiotensin II, and thromboxane A2, which have smooth muscle contractile properties, can also interfere withsmooth muscle relaxation and prevent erection.

  • Figure 4. Relaxation of Penile Smooth Muscle via cGMP Pathway

    Figure 4.

    Relaxation of Penile Smooth Muscle via cGMP Pathway

    (Enlarge Slide)