Background and purpose: Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that prevents the fructose-induced arterial stiffening in male Wistar rats. Our aims were to examine whether AG produced benefits on the left ventricular (LV)-arterial coupling in fructose-fed (FF) animals in terms of the ventricular and arterial chamber properties. Experimental approach: Rats given 10% fructose in drinking water (FF) were daily treated with AG (50 mg Á kg À1 , i.p.) for 2 weeks and compared with the untreated FF group. In anaesthetised rats, LV pressure and ascending aortic flow signals were recorded to calculate LV end-systolic elastance (E es , an indicator of myocardial contractility) and effective arterial volume elastance (E a ). The optimal afterload (Q load ) determined by the ratio of E a to E es was used to measure the coupling efficiency between the left ventricle and its vasculature. Key results: There was a significant interaction between fructose and AG in their effects on E a . Fructose loading significantly elevated E a and AG prevented the fructose-derived deterioration in arterial chamber elastance. Both fructose and AG affected E es and Q load , and there was an interaction between fructose and AG for these two variables. Both E es and Q load exhibited a decline with fructose feeding but showed a significant rise after AG treatment in the FF rats. Conclusions and Implications: AG prevented not only the contractile dysfunction of the heart caused by fructose loading, but also the fructose-induced deterioration in matching left ventricular function to the arterial system. Keywords: aminoguanidine; effective arterial volume elastance; fructose loading; end-systolic elastance; ventricular-arterial coupling Abbreviations: AG, aminoguanidine; AGEs, advanced glycation endproducts; BW, body weight; CO, cardiac output; E a , effective arterial volume elastance; E es , left ventricular end-systolic elastance; HR, basal heart rate; LVW, left ventricular weight; P es , end-systolic pressure of the left ventricle; P isomax , peak isovolumic pressure of the left ventricle; Q load , optimal afterload; SV, stroke volume; V ed , end-diastolic volume of the left ventricle; V eed , effective end-diastolic volume of the left ventricle; V 0 , the zero-pressure volume