Abstract
Zaher Armaly1 and Zaid Abassi2,3* 1Departmentof Nephrology, EMMS Nazareth–The Nazareth Hospital, Nazareth and Galilee Medical School-Bar Ilan University, Safed, Israel 2Research Unit, Rambam Health Care Campus Haifa, Israel 3Department of Physiology, Rappaport Faculty of Medicine, Technion–Israel Institute of Technology, Haifa, Israel *Corresponding author: Zaid Abassi, Department of Physiology & Biophysics, Rappaport Faculty of Medicine, Technion, IIT, P.O.B 9649, Haifa 31096, Israel, Tel: 972-4-8295-267; Fax: 972-4-8295-266; E-mail: abassi@tx.technion.ac.il
Highlights
Introduction summarized by Reffelmann andKloner [2], the current communication will concisely focus on recent studies that supportSildenafil, the oldest approved Phosphodiesterase 5 (PDE5) potential nephroprotective profiles of PDE5 inhibitors in both inhibitor, was originally developed for the treatment of angina pectoris experimental and clinical research
The relaxation of renal vasculature as determined in isolated perfused kidneys was reduced in these mice. 2-Kidney-1-Clip-Operation (2K1C) operated Wild Type (WT) mice showed a reduction of cyclic Guanosine Monophosphate (cGMP)-dependent relaxation of renal vessels, which was not found in the Nitric Oxide (NO)-GC1 KOs
The initial application of PDE5 inhibitor for erectile dysfunction has evolved to other clinical settings including heart failure, pulmonary hypertension and kidney dysfunction
Summary
AKI: Acute Kidney Injury; BNP: Brain Natriuretic Peptide; cGMP: Cyclic Guanosine Monophosphate; CKD: Chronic Kidney Disease; GFR: Glomerular Filtration Rate; KIM-1: Kidney Injury Molecule 1; iNOS: Inducible NO Synthase; PUUO: Partial Unilateral Ureteral Obstruction; I/R: Ischemia-Reperfusion; MB: Mitochondrial Biogenesis; NGAL: Neutrophil Gelatinase Associated Lipocaline; NO: Nitric Oxide; PDE5: Phosphodiesterase 5; TGF-β: Transforming Growth Factor Beta. This approach may suggest a prophylactic therapy for patients with ischemic AKI These results are in agreement with other studies that reported beneficial renal effects of PDE5 inhibitors in the I/R rat model [22,23], after unilateral ureteral obstruction [24], following cardiopulmonary bypass AKI in swine [25], and post-transplant of warm ischemic kidney [26]. While these studies examined the effects of PDE5 inhibitor pre-treatment on renal histology, oxidative stress, and function, our study [17] assessed the effects of PDE5 inhibitors on the more sensitive biomarkers of AKI [18,19,20,21], namely NGAL and KIM-1. PDE5 inhibition induce anti-apoptotic effects, [31,36] antioxidative stress [37] and anti-inflammation [38] on renal cells in CKD models [33]
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