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. 2008 Oct 16;118(11):3701–3713. doi: 10.1172/JCI35470

Figure 1. Response to vasoconstrictive agents in the femoral arteries from control (WT), Abcg1–/–, Abca1–/–, and Abca1–/–Abcg1–/– mice.

Figure 1

(A–C) WT and Abcg1–/– mice (n = 4 per group) were put on a HCD (1.25% cholesterol, 7.5% cocoa butter and 0.5% sodium cholate) for 11 weeks. (A) Original trace recordings showing vessel tension increase after addition of 3 μM phenylephrine (PE) and relaxation in response to different concentrations of ACh. ACh-induced vasorelaxation occurred at the indicated concentrations in control and Abcg1–/– mice. (B) Vasorelaxation in response to ACh was markedly attenuated in Abcg1–/– mice. (C) There was no significant difference in relaxation in response to SNP. (D and E) WT and Abcg1–/– mice (n = 5 per group) were put on a chow diet. There was no difference between the groups in the response to ACh (D) or SNP (E). (F and G) WT, Abcg1–/–, Abca1–/–, and Abca1–/–Abcg1–/– (n = 5 per group) were put on a WTD (0.25% cholesterol and 21% milk fat) for 12 weeks. (F) There was a similar severe defect in vascular relaxation response to ACh in Abcg1–/– and Abca1–/–Abcg1–/– mice, while the response of Abca1–/– mice was intermediate between these groups and the controls. (G) There was no significant difference in relaxation in response to SNP. The results are represented as mean ± SEM.