Fig. 5

Tempol 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 incubation with high glucose (HG, 30 mM) and methylglyoxal (MGO, 120 µM) in absence and presence of tempol (Temp, 100 µM) after precontraction with Phe (10 µM for mesenteric arteries; 5 µM for corpora cavernosa). c Electrical field stimulated (EFS) relaxations of 5 µM Phe-precontracted mouse corpora cavernosa after 2 h incubation with high glucose (HG, 30 mM) and methylglyoxal (MGO, 120 µM) in absence and presence of tempol (Temp, 100 µM). Data are expressed as % decrease of Phe-induced tone; Mann–Whitney U test; ^#p < 0.01 and *p < 0.05 (n = 5–6)