Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.

39 – 43 When comparing AngII-infused cells to saline-infused controls generating similar magnitude I Ca (and, thus, presumably similar calcium-dependent inactivation), we observed a trend toward slower channel inactivation in the AngII-infused cells though this did not reach statistical significance when accounting for animal-to-animal variability (Figure 3 C and 3 H).

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