Erectile Dysfunction: Epidemiology, Physiology, and Etiologies

2019 ◽  
Author(s):  
Jonathan Fainberg ◽  
James A Kashanian

ED is defined as the consistent inability to achieve or maintain an erection adequate for sexual activity. It is a widely prevalent disease, affecting approximately 20 million men in the United States alone. ED rates increase as men get older; however, ED is not necessarily a normal part of aging. Early-onset ED has been a predictor of underlying cardiovascular diseases, and most clinicians now advocate for a cardiology evaluation in men with new-onset organic ED. The most common etiology of ED is a vascular disease; however, ED can be caused by diabetes, endocrinopathies, medications, chronic illness, and trauma. Psychogenic causes of ED are also common. Physiology of the penile erection is complicated; however, its comprehensive understanding is imperative to enable a proper etiologic diagnosis of ED. Blood supply to the penis originates from the hypogastric arterial system, and nitric oxide is the primary neurotransmitter involved in penile erections. The epidemiology, physiology, and etiologies of erectile dysfunction are discussed in detail in this chapter. This review contains 1 figure, 2 tables, and 50 references. Key Words: causes of erectile dysfunction, epidemiology of erectile dysfunction, erectile dysfunction, nitric oxide, phosphodiesterase-5 inhibitors, physiology of the penile erection, psychogenic erectile dysfunction, sexual dysfunction, cyclic guanosine monophosphate, detumescence.

Author(s):  
Thomas J Pirtle ◽  
Richard A Satterlie

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.


2011 ◽  
Vol 89 (2) ◽  
pp. 89-95 ◽  
Author(s):  
Ercan Ozdemir ◽  
Ihsan Bagcivan ◽  
Nedim Durmus ◽  
Ahmet Altun ◽  
Sinan Gursoy

Although the phenomenon of opioid tolerance has been widely investigated, neither opioid nor nonopioid mechanisms are completely understood. The aim of the present study was to investigate the role of the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway in the development of morphine-induced analgesia tolerance. The study was carried out on male Wistar albino rats (weighing 180–210 g; n = 126). To develop morphine tolerance, animals were given morphine (50 mg/kg; s.c.) once daily for 3 days. After the last dose of morphine was injected on day 4, morphine tolerance was evaluated. The analgesic effects of 3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1), BAY 41-2272, S-nitroso-N-acetylpenicillamine (SNAP), NG-nitro-l-arginine methyl ester (L-NAME), and morphine were considered at 15 or 30 min intervals (0, 15, 30, 60, 90, and 120 min) by tail-flick and hot-plate analgesia tests (n = 6 in each study group). The results showed that YC-1 and BAY 41-2272, a NO-independent activator of soluble guanylate cyclase (sGC), significantly increased the development and expression of morphine tolerance, and L-NAME, a NO synthase (NOS) inhibitor, significantly decreased the development of morphine tolerance. In conclusion, these data demonstrate that the nitric oxide–cGMP signal pathway plays a pivotal role in developing tolerance to the analgesic effect of morphine.


2010 ◽  
Vol 58 (4) ◽  
pp. 616-625 ◽  
Author(s):  
Romain Caremel ◽  
Stephanie Oger-Roussel ◽  
Delphine Behr-Roussel ◽  
Philippe Grise ◽  
François A. Giuliano

2000 ◽  
Vol 6 (5) ◽  
pp. 404-414 ◽  
Author(s):  
Irina A. Buhimschi ◽  
Chandreskar Yallampalli ◽  
Catalin S. Buhimschi ◽  
George R. Saade ◽  
Robert E. Garfield

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