Effect of paricalcitol on cardiac dysfunction parameters.

<p>(A) Representative hearts in 1α-OHase^−/− mice with or without PC treatment after 4 weeks of sham or TAC. (B) HW/BW ratio in 1α-OHase^−/− mice with or without PC treatment after 4 weeks of sham or TAC. *, <i>p</i><0.05 compared to Sham. #, <i>p</i><0.05 compared to vehicle TAC. N = 8–10. (C) Representative Masson-Trichrome heart staining in 1α-OHase^−/− mice with or without PC treatment after 4 weeks of sham or TAC. (D and E) Real-time PCR mRNA expression of ANF (D) and of ß-MHC to total MHC ratio (E) after 4 weeks of sham or TAC in 1α-OHase^−/− mice with or without PC treatment. *, <i>p</i><0.05 compared to Sham. #, <i>p</i><0.05 compared to vehicle TAC. N = 8–10. (F–H) Fractional shortening (F), stroke volume (G) and cardiac output (H) in 1α-OHase -/- mice with or without PC treatment after 4 weeks of sham or TAC. *, <i>p</i><0.05 compared to Sham. #, <i>p</i><0.05 compared to vehicle TAC. N = 8–10. Effect of paricalcitol on defective calcium handling in 1αOHase −/− mice. (I–L). The % peak Ca²⁺ (I), % peak shortening (J), the rate of Ca²⁺ transient decay (<i>Tau</i>) (K), and the return velocity to baseline or Ca²⁺ efflux (L) in 1α-OHase^−/− mice with or without PC treatment. *, <i>p</i><0.05 compared to vehicle treated mice group, N = 20 CMs/mouse from 6–8 mice/group.