title: 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 (tau), from 22.6 +/- 0.6 to 19.2 +/- 0.7 msec (P < 0.05). The elevated Z(c) and the reduced tau 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 tau (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.
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University, No. 1, Sec. 1, Jen-Ai Road, Taipei, Taiwan.
authors.forename: Yi-Tsen
authors.initials: YT
authors.lastname: Lin
authors.forename: Yung-Zu
authors.initials: YZ
authors.lastname: Tseng
authors.forename: Kuo-Chu
authors.initials: KC
authors.lastname: Chang
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology; D002302:Cardiac Output / Q000187:drug effects; D017097:Electric Impedance; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D005632:Fructose / Q000008:administration & dosage / Q000494:pharmacology*; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors; D006146:Guanidines / Q000008:administration & dosage / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D008297:Male; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004791:Enzyme Inhibitors; D017127:Glycation End Products, Advanced; D006146:Guanidines; D005632:Fructose; C004479:pimagedine