Fig. 4

Ascorbic acid prevents high glucose and methylglyoxal-induced deficits in mesenteric artery and corpora cavernosa. Acetylcholine (Ach)-induced relaxations of a mesenteric artery and b corpora cavernosa after 2 h co-incubation with high glucose (HG, 30 mM) and methylglyoxal (MGO, 120 µM) in absence and presence of ascorbic acid (AA, 100 µM) after precontraction with Phe (10 µM for mesenteric arteries; 5 µM for corpora cavernosa). c Electrical field stimulated (EFS) relaxations of corpora cavernosa after 2 h incubation with high glucose (HG, 30 mM) and methylglyoxal (MGO, 120 µM) in absence and presence of ascorbic acid (AA, 100 µM). Data are expressed as % decrease of Phe-induced tone; Mann–Whitney U test; ^#p < 0.01 and *p < 0.05 (n = 5–7)