ORIGINAL ARTICLE Acetylsalicylic acid protects erectile function in diabetic rats G. Hafez 1 , U. Gonulalan 2 , M. Kosan 2 , E. Arioglu 1 , B. Ozturk 2 , M. Cetinkaya 3 & S. Gur 1 1 Faculty of Pharmacy, Department of Pharmacology, Ankara University, Ankara, Turkey; 2 Department of Urology, Baskent University, Konya Research and Training Hospital, Konya, Turkey; 3 Department of Urology, Ankara Numune Education and Research Hospital, Ankara, Turkey Keywords Acetylsalicylic acid—diabetes mellitus—erec- tile dysfunction—in vitro—intracavernosal pressure Correspondence Umut Gonulalan, School of Medicine, Baskent University, Konya Research and Training Hospital, Saray Street, No: 1 Selcuklu, Konya, Turkey. Tel.: +90 332 2631494; Fax: +90 332 2570637; E-mail: drugonulalan@yahoo.com Accepted: September 16, 2013 doi: 10.1111/and.12187 Summary We aimed to evaluate the effect of acetylsalicylic acid (ASA) treatment on dia- betes-induced erectile dysfunction. Adult male Sprague–Dawley rats were divided into four groups as follows: (i) control (C), (ii) diabetic (D), (iii) ASA-treated control (C+ASA) and (iv) ASA-treated diabetic (D+ASA) groups. In groups 2 and 4, diabetes was induced by injection of 35 mg kg À1 streptozo- tocin. ASA (100 mg kg À1 day À1 , orally) was administrated to rats in groups 3 and 4 for 8 weeks. Both intracavernosal pressure (ICP) and mean arterial blood pressure (MAP) were measured in in vivo studies. In organ bath, the relaxation responses to acetylcholine (ACh), electrical field stimulation (EFS) and sodium nitroprusside were tested in corpus cavernosum (CC) strips. The mRNA expression for neuronal nitric oxide synthase (nNOS) was calculated using reverse transcription polymerase chain reaction technique. In in vivo experi- ments, diabetic rats displayed reduced ICP/MAP values, which were normalised with ASA treatment. The relaxant response to high-dose ACh and EFS at low frequencies (1–8 Hz) in CC strips from the D+ASA group were significantly higher when compared to the D group. Treatment with ASA normalised the raised mRNA expressions of nNOS in diabetic penile tissues. ASA may be involved in mRNA of protein synthesis of NO released from nonadrenergic and noncholinergic cavernosal nerve in diabetes. Introduction Penile erection is in control of a complex neural and vas- cular interaction that causes cavernosal smooth muscle relaxation. The nitric oxide (NO) is synthesised by neuro- nal (nNOS) and endothelial NO synthase (eNOS) and plays an important role in cavernosal smooth muscle relaxation with the NO/cyclic guanosine monophosphate (cGMP) cascade (Rajfer et al., 1992; Toda et al., 2005). Diabetes mellitus (DM) is the common risk factor for erectile dysfunction (ED), although the pathogenesis of ED in DM remains controversial because of the multifac- torial nature of DM (Sasaki et al., 2003). The neuropathy and vascular dysfunction make it difficult to pinpoint a single aetiology for ED (Bennett et al., 2005). Acetylsalicylic acid (ASA) acts with significant efficacy in the treatment of coronary and cerebrovascular events (Awtry & Loscalzo, 2000). This effect is a result of cyclooxygenase-1 inhibition in platelets and endothelium- dependent arterial relaxation (Awtry & Loscalzo, 2000; Monobe et al., 2001). In a recent report, ASA improved endothelium-dependent vasorelaxation through increased bioavailability of NO (Tauseef et al., 2008). On the other hand, indomethacin and diclofenac as nonsteroidal anti- inflammatory drugs negatively affected the erectile pro- cess in rats due to reduction in the plasma level of NO (Senbel, 2011). nNOS is localised in penile autonomic nerves and arterioles. However, eNOS is detectable in endothelial cells of the corpus cavernosum (CC) (Anders- son & Wagner, 1995). Both reduction in nNOS expres- sion and endothelial morphological changes have been documented as causing ED in diabetes (Albersen et al., 2011). To date, there has been no study regarding treatment of ED with ASA in diabetic rats. The goal of the current study was to investigate the effect of ASA treatment on © 2013 Blackwell Verlag GmbH 997 Andrologia 2014, 46, 997–1003