Figure 7

Frequency domain HRV analysis in constitutive and ventricle-specific Girk^−/− mice. (a) Power in the VLF ( < 0.4 Hz) range at baseline and following injection of CCh (1.0 mg/kg i.p.). Two-way ANOVA analysis revealed an interaction between genotype and treatment (F_1,23 = 36.3, P < 0.001) for wild-type (n = 12) and Girk4^−/− (n = 13) mice (left panel). While main effects of treatment (F_1,23 = 51.0, P < 0.001) and genotype (F_1,23 = 13.77, P < 0.01) were observed for MLC2VCre(−):Girk1^fl/fl (n = 13) and MLC2VCre(+):Girk1^fl/fl (n = 12) mice (right panel), there was no interaction between genotype and treatment (F_1,23 = 0.01, P = 0.90). Symbols: ***P < 0.001 vs. baseline (within genotype); ^###P < 0.001 vs. wild-type (within treatment). (b) Power in the LF (0.4–1.5 Hz) range at baseline and following injection of CCh (1.0 mg/kg i.p.). Two-way ANOVA analysis revealed an interaction between genotype and treatment (F_1,23 = 41.6, P < 0.001) for wild-type and Girk4^−/− mice (left panel). While main effects of treatment (F_1,23 = 113.1, P < 0.001) and genotype (F_1,23 = 8.8, P < 0.01) were observed for MLC2VCre(−):Girk1^fl/fl and MLC2VCre(+):Girk1^fl/fl mice (right panel), there was no interaction between genotype and treatment (F_1,23 = 0.02, P = 0.88). Symbols: ***P < 0.001 vs. baseline (within genotype); ^##,###P < 0.01 and 0.001, respectively, vs. wild-type (within treatment). (c) Power in the HF (1.5–5.0 Hz) range at baseline and following injection of CCh (1.0 mg/kg i.p.). Two-way ANOVA analysis revealed an interaction between genotype and treatment (F_1,23 = 37.5, P < 0.001) for wild-type and Girk4^−/− mice (left panel). There were no main effects of treatment (F_1,23 = 2.7, P = 0.11) or genotype (F_1,23 = 1.8, P = 0.19) for MLC2VCre(−):Girk1^fl/fl and MLC2VCre(+):Girk1^fl/fl mice (right panel), nor was there an interaction between genotype and treatment (F_1,23 = 0.8, P = 0.38). Symbols: ***P < 0.001 vs. baseline (within genotype). ^##P < 0.01 vs. wild-type (within treatment).