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Materials and methods Wistar rats (n = 10–14 per group) were fed a standard chow (CONT) or a 60% fructose/5% fat (% by weight)enriched diet for 8 weeks (FFR). From week 5 through 8, sildenafil was administered twice a day (sc, 20 mg/kg, FFR+SIL), thus reaching clinically relevant plasma concentrations circa 20 nM unbound known to give efficacy in man (Pfizer Inc., data on file), then a 1-week wash-out period from sildenafil was observed. Isometric tension studies were performed on isolated aortic and superior mesenteric arterial (SMA) rings precontracted with noradrenaline to build concentration-response curves (CRC) to endothelium-dependent (ACh and A23187) and -independent (SNP) relaxants in presence of indomethacin. Urinary 8-isoprostanes (IPT) and plasma levels of IL-6 and TNF-α were also evaluated. Results Relaxations to ACh were reduced in aortas of FFR (10-5 M: -102.6 ± -2.4% vs -89.2 ± 4.7, p < 0.001) while only slightly affected in SMA rings. Relaxations to A23187 were significantly reduced both in aortic and SMA rings of FFR. In aortas, sildenafil treatment restored normal endothelium-dependent relaxations to ACh (10-5 M: -104.2 ± 3.0%, p < 0.001) even after one week of wash-out from treatment. In SMA rings, a leftward shift of the CRC to ACh could be detected (pD2: -8.12 ± 0.11 vs -8.60 ± 0.08, p < 0.05). Relaxations to A23187 were also restored by sildenafil in both aortic and SMA rings of FFR. Enhanced compensatory endothelium-independent relaxations to SNP in FFR were not modified by sildenafil treatment. Neither IL-6 nor TNF-α were modified by the fructose or sildenafil treatment. Urinary IPT levels was normalized by the sildenafil treatment (FFR: 2.07 ± 0.36 vs CONT:0.95 ± 0.14 vs FFR+SIL: 0.88 ± 0.13 ng/ml/24 h, p < 0.05).

bmc pharmacology

Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses endothelial dysfunction and oxidative stress associated with the metabolic syndrome