Figure 7. The strain-specific hypertension in sGCα₁^–/– mice is associated with greater impairment of vascular reactivity in sGCα₁^–/–S6 mice than in sGCα₁^–/–B6 mice.

Acetylcholine-induced relaxation was studied in phenylephrine-precontracted aortic rings from male wild-type (black symbols, solid line) and sGCα₁-deficient mice (sGCα₁^–/–) on a B6 (circles) or S6 (squares) genetic background. sGCα₁^–/– mice were either pretreated (gray symbols, dashed line) or not (white symbols, dotted line) with the ACE inhibitor (ACEI) enalapril. Acetylcholine-induced vascular relaxation was impaired to a greater extent in sGCα₁^–/–S6 than in sGCα₁^–/–B6 mice. In vivo pretreatment with enalapril restored vascular reactivity in sGCα₁^–/–S6 to levels observed in sGCα₁^–/–B6 mice. n = 9, 8, 9, 4, 10, and 12 for sGCα₁^–/–S6, sGCα₁^–/–B6, sGCα₁^–/–S6ACEI, sGCα₁^–/–B6 ACEI, WT^S6, and WT^B6, respectively. *P < 0.001 versus sGCα₁^–/–S6; ^†P < 0.01 versus sGCα₁^–/–B6; ^‡P < 0.05 versus sGCα₁^–/–S6; ^§P < 0.01 versus sGCα₁^–/–S6.