Grape Seed Extract Polyphenols Improve Resistance Artery Function in Pregnant eNOS–/– Mice

Figures

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  FIGURE 1. GSEP supplementation lowers systolic blood pressure without affecting heart rate in eNOS–/– mice at GD17.5. In eNOS–/– mice, systolic blood pressure (SBP) was significantly higher compared with WT animals, and was reduced by supplementation with GSEP (A). Heart rate (HR) was significantly lower in eNOS–/– mice compared with WT animals but was unaffected by GSEP treatment (B). #P < 0.05 eNOS–/– vs. WT; **P < 0.01 GSEP vs. H2O. N = 3–4 dams per group.

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  FIGURE 2. Treatment with GSEP decreases oxidative stress in maternal plasma of eNOS–/– mice. Concentrations of malondialdehyde (MDA) were significantly higher in maternal plasma of eNOS–/– mice compared with WT H2O mice and were significantly reduced in eNOS–/– mice treated with GSEP. #P < 0.05 eNOS–/– vs. WT H2O; **P < 0.01 GSEP vs. H2O. N = 5–6 dams per group.

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  FIGURE 3. Supplementation with GSEP has no effect on maximal smooth muscle depolarization. Treatment with GSEP did not alter constriction of either aortas (A), mesenteric (B), or uterine (C) arteries in response to a maximal smooth muscle depolarization induced by KPSS in WT or eNOS–/– mice. ##P < 0.01, ###P < 0.001 eNOS–/– vs. WT. N = 6–11 dams per group.

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  FIGURE 4. GSEP supplementation increases thromboxane mimetic-induced constriction of uterine arteries in eNOS–/– mice. Aortas of eNOS–/– mice (A), but not mesenteric (D) or uterine arteries (G), showed significantly higher constriction to U46619 compared with WT controls. Maternal GSEP supplementation did not affect constriction in response to U46619 of either aortas (B,C) or mesenteric arteries (E,F) in WT or eNOS–/– mice. In uterine arteries, GSEP treatment had no effect on U46619-induced constriction in WT (H) but significantly increased vasoconstriction in eNOS–/– mice (I). ##P < 0.01 eNOS–/– vs. WT; ****P < 0.0001 GSEP vs. H2O. N = 6–11 dams per group.

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  FIGURE 5. GSEP supplementation improves endothelium-dependent relaxation of mesenteric and uterine arteries in eNOS–/– mice. In eNOS–/– mice, aortas did not relax in response to ACh (A,C) and endothelium-dependent relaxation was significantly reduced in both mesenteric (D) and uterine (G) arteries compared with WT controls. Supplementation with GSEP had no effect on endothelium-dependent relaxation to ACh in aortas of WT mice (B). In both mesenteric and uterine arteries, relaxation to ACh was unaffected by GSEP in WT mice (E,H, respectively) but was significantly enhanced in eNOS–/– mice (F,I, respectively). ####P < 0.0001 eNOS–/– vs. WT; *P < 0.05, ***P < 0.001 GSEP vs. H2O. N = 6–11 dams per group.

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  FIGURE 6. Treatment with GSEP enhances endothelium-independent relaxation of uterine arteries in eNOS–/– mice. Endothelium-independent relaxation in response to SNP was significantly increased in aortas of eNOS–/– mice compared with WT controls (A), but did not change between genotypes in either mesenteric (D) or uterine arteries (G). Supplementation with GSEP had no effect on responses to SNP in either aortas (B,C) or mesenteric arteries (E,F) from WT and eNOS–/– mice. In uterine arteries, the treatment had no effect in WT (H) but significantly improved relaxation to SNP in eNOS–/– mice (I). ###P < 0.001 eNOS–/– vs. WT; *P < 0.05 GSEP vs. H2O. N = 6–11 dams per group.

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  FIGURE 7. Treatment with GSEP normalizes diameter of posterior cerebral arteries in eNOS–/– mice. Increasing intraluminal pressure (10–110 mmHg) significantly expanded lumen diameters of fully dilated posterior cerebral arteries of eNOS–/– mice compared with WT controls (A). Treatment with GSEP had no effect on lumen diameters of WT mice (B), but significantly reduced diameters in eNOS–/– mice (C). Distensibility (D) but not circumferential wall stress (E) at 110 mmHg was significantly affected by the treatment. ##P < 0.01 eNOS–/– vs. WT;*P < 0.05; ***P < 0.001 GSEP vs. H2O. N = 6–9 dams per group.