Aminoguanidine Prevents Fructose-Induced Arterial Stiffening in Wistar Rats: Aortic Impedance Analysis

Abstract

Fructose has been reported as a potent agent in forming advanced glycation end products (AGEs) and, thus, may play a significant role in the pathogenesis of diabetic complications. Herein, we determined the effects of aminoguanidine (AG), an inhibitor of AGEs, on the mechanical properties of the arterial system in fructose-fed (FF) rats, using aortic impedance analysis. Rats at 2 months were given 10% fructose in drinking water for 2 weeks and compared with untreated age-matched controls. Meanwhile, FF rats were treated for 2 weeks with AG (daily peritoneal injections of 50 mg kg⁻¹) and compared with the untreated FF group. Neither fructose nor AG affects body weight, blood glucose level, and basal heart rate. In comparison with controls, FF rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance (R_p), at 51.1 ± 2.9 versus 66.2 ± 1.9 mm Hg sec ml⁻¹ (P < 0.05). Fructose also contributed to an increase in aortic characteristic impedance (Z_c), from 1.528 ± 0.094 to 1.933 ± 0.084 mm Hg sec ml⁻¹ (P < 0.05) and a decrease in wave transit time (τ), from 22.6 ± 0.6 to 19.2 ± 0.7 msec (P < 0.05). The elevated Z_c and the reduced τ suggest that fructose may cause a detriment to the aortic distensibility in animals. After exposure to AG, FF rats exhibited a significant improvement in physical properties of the resistance vessels, as evidenced by the reduction of 21.3% in R_p. Meanwhile, AG retarded the fructose-induced decline in aortic distensibility, as reflected in the decrease of 16.0% in Z_c (P < 0.05) and the increase of 18.1% in τ (P < 0.05). By contrast, AG exerted no effects on the mechanical properties of Windkessel vessels, as well as resistance vessels, in normal diet controls. We conclude that AG may prevent the fructose-derived changes in arterial stiffening, possibly through inhibition of the fructose-derived advanced glycation end product formation in Wistar rats.