Fig. 4

Vascular nitric oxide (NO) signaling. a Schematic illustration of the experimental setup. Porcine coronary artery segments were mounted under 40 mN resting tension in an organ bath and pre-contracted with PGF2α (= baseline). NO-mediated dilatory responses were recorded after injection of the NO donor MAHMA-NONOate (30 nM) into the immersion buffer. b Hb (32 μM) but not Hb complexes with predominantly human plasma derived (pd) Hp 2–2 blunted the dilatory response. c and d Wild-type rHp variants preserved vascular NO-signaling comparable to plasma derived Hp. In contrast, intermediate dilatory responses were observed in the presence Hb mixed with cleavage site mutated rHp variants. The traces show mean +/− SEM of at least 6 averaged responses recorded in three independent experiments. e ANOVA statistics of the AUCs of the dilatory responses recorded in the different experiments. Non-overlapping circles indicate significantly different responses at p < 0.05 (Tukey-Kramer post-test)