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. 2013 Feb 1;304(7):H935–H945. doi: 10.1152/ajpheart.00513.2012

Fig. 3.

Fig. 3.

Diabetes in rat pregnancy markedly impairs EDHF-mediated uteroplacental vasodilation to ACh. A and B: summary graphs showing the degree of T and S EDHF-mediated vasodilation as a function of ACh concentrations in arteries from control and diabetic rats pretreated with N-nitro-l-arginine (l-NNA; 200 μM) and indomethacin (10 μM). ACh-induced vasodilation is expressed as Dmax. *Significantly different compared with the respective control group at P < 0.05 (by two-way repeated-measures ANOVA). C and D: bar graphs showing the marked increase in ACh EC50 concentrations for T and S vasodilation in uterine arteries of diabetic [−6.29 ± 0.15 and −6.42 ± 0.21 log(ACh), in M] versus control [−6.89 ± 0.09 and −6.99 ± 0.13 log(ACh), in M] rats. *Significantly different compared with the respective control group at P < 0.05 (by unpaired Student's t-test). Numbers in parentheses indicate the numbers of arteries tested.