FIGURE 3.

l‐cysteine‐ and NaHS‐induced increase in tension involves the eNOS/sGC/NO pathway. (a) l‐cysteine‐ and (b) NaHS‐induced contraction on phenylephrine (PE)‐precontracted aortic rings was abolished in aorta harvested from eNOS^−/− (n = 7 mice l‐cysteine, n = 6 mice NaHS) and sGC_α1 ^−/− mice (n = 7 mice l‐cysteine, n = 9 mice NaHS) compared to WT mice (n = 7 mice l‐cysteine, n = 9 mice NaHS). (c) l‐cysteine‐induced contraction is abolished in PE‐precontracted aortic rings incubated with l‐NIO (10 μM, 20 min; n = 5 mice) or ODQ (10 μM, 15 min; n = 8 mice) compared to vehicle (n = 8 mice). (d) NaHS‐induced contraction is abolished in PE‐precontracted aortic rings incubated with l‐NIO (10 μM, 20 min; n = 6 mice) or ODQ (10 μM, 15 min; n = 6 mice) compared to vehicle (n = 8 mice). Values shown are means ± SEM and are expressed as δ increase in tension over PE contraction (dyne/mg tissue). *P < 0.05 significantly different as indicated; two‐way ANOVA with Bonferroni's post hoc test