Figure 5. Analysis of intracellular Ca²⁺ and Na⁺ handling in adult myocytes from NKA-α1 and NKA-α2 transgenic mice.

A, Mean amplitude of Ca²⁺ transients measured from Wt, NKA-α2, and high-line NKA-α1 isolated transgenic cardiomyocytes paced at 0.5 Hz. B, Sarcoplasmic reticulum (SR) Ca²⁺ load measured from Wt, NKA-α2, and high-line NKA-α1 isolated transgenic cardiomyocytes via caffeine-induced Ca²⁺ release. C,D, [Na⁺]_i measured from Wt, NKA-α2, and high-line NKA-α1 isolated transgenic cardiomyocytes under resting conditions (C), and during stimulation at 2 Hz (D). Number of myocytes analysed is given within the graph. *P<0.05 versus WT. E, Rate of [Ca²⁺]_i decline after caffeine-induced depletion of SR stores measured from Wt, NKA-α2, and NKA-α1 transgenic myocytes either in the presence of 10 mM NiCl₂ (to block NCX1) or in the absence of NiCl₂ (control). *P<0.05 versus control (no nickel); #P<0.05 vs Wt of same treatment. F, Immunoblots of phosphoprotein and total protein levels for the indicated Ca²⁺ and Na⁺ handling proteins from cardiac homogenates of Wt, high-line NKA-α1 transgenic or NKA-α2 transgenic hearts after 16 weeks of TAC or sham surgery. For each experiment, the number of mice analyzed is given in the graph. Quantitation of the data are shown in Online Figure IV. *P<0.05 versus sham; #P<0.05 vs Wt TAC.