Abstract
Erectile dysfunction (ED) is a prevalent condition, especially in men over 40 years old, characterized by the inability to obtain and/or maintain penile erection sufficient for satisfactory sexual intercourse. Several psychological and/or organic factors are involved in the etiopathogenesis of ED. In this context, we gathered evidence of the involvement of Large-conductance, Ca2+-activated K+ channels (BKCa), Small-conductance, Ca2+-activated K+ channels (SKCa), KCNQ-encoded voltage-dependent K+ channels (KV7), Transient Receptor Potential channels (TRP), and Calcium-activated Chloride channels (CaCC) dysfunctions on ED. In addition, the use of modulating agents of these channels are involved in relaxation of the cavernous smooth muscle cell and, consequent penile erection, suggesting that these channels are promising therapeutic targets for the treatment of erectile dysfunction.
Highlights
Erectile dysfunction (ED) is a persistent inability to achieve and/or maintain a penile erection enough for satisfactory sexual intercourse (McCabe et al, 2016)
Multifactorial nature of ED is evident and, population studies have shown that several conditions involving vascular abnormalities such as hypertension, aging, physical inactivity, dyslipidemia, diabetes, insulin resistance, and obesity are among the major risk factors that favor the development of ED in man and animal models (Musicki et al, 2010; Kaya et al, 2015; Maseroli et al, 2015)
Other mediators are responsible for modulating cavernous smooth muscle relaxation, such as prostacyclin (PGI2) and type 1 and 2 prostaglandins (PGE1 and PGE2). These prostanoids act on the Gs protein-coupled IP, EP2 and EP4 receptors, culminating in activation of Cyclic guanosine monophosphate (cGMP) and cAMPdependent protein kinases (PKG and Cyclic adenosine monophosphate (cAMP) dependent protein kinase (PKA), respectively) which, when activated, phosphorylate various targets such as potassium channels, activating them, and voltage-dependent calcium channels, inhibiting them (Figure 1) (Porst, 1996; Angulo et al, 2002; Andersson, 2011)
Summary
Erectile dysfunction (ED) is a persistent inability to achieve and/or maintain a penile erection enough for satisfactory sexual intercourse (McCabe et al, 2016). In recent years, researching involving the flaccidity and penile erection has focused mainly on molecular mechanisms. In this sense, several neurotransmitters, second messengers, reactive oxygen species (ROS), growth factors, hormones, and ion channels have been characterized as important components of the complex erection process, leading to the discovery of new therapeutic targets for the treatment of ED. This review will focus on providing an update on the importance of some ion channels involved in the regulation of intracellular signaling and tone of cavernous smooth muscle and their potential as therapeutic targets to the development of new drugs to treatment of erectile dysfunction. Aging is the major risk factor for ED and both the prevalence and severity of the disease increase with aging, so it is usually caused by the presence of neural and endothelial dysfunction (El-Sacca, 2007; Lewis et al, 2012)
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