Aminoguanidine prevents fructose-induced arterial stiffening in Wistar rats: Aortic impedance analysis
Journal
Experimental Biology and Medicine
Journal Volume
229
Journal Issue
10
Pages
1038-1045
Date Issued
2004
Author(s)
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 (Rp), 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 (Zc), 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 Zc 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 Rp. Meanwhile, AG retarded the fructose-induced decline in aortic distensibility, as reflected in the decrease of 16.0% in Zc (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.
Subjects
Advanced glycation end products; Aminoguanidine; Aortic input impedance; Fructose; Pulse wave reflection
SDGs
Other Subjects
advanced glycation end product; aminoguanidine; drinking water; fructose; glucose; animal experiment; aorta; artery dilatation; article; body weight; controlled study; drug exposure; feeding; glucose blood level; heart output; heart rate; impedance; male; mean arterial pressure; nonhuman; rat; rigidity; spectral sensitivity; vascular resistance; Animalia; Rattus norvegicus
Publisher
Society for Experimental Biology and Medicine
Type
journal article