Figure 1.

Cardiomyocyte Ca²⁺ transients and sparks with nitric oxide donor S-nitrosoglutathione (GSNO). A, Nitric oxide (NO) liberated from increasing GSNO concentrations in buffer was measured using a NO electrode. B, The kinetics of NO release following the addition of 150 μM GSNO to buffer. C, Western blot of ventricle tissue samples from wild-type (WT) and CaMKIIδ (Ca²⁺/calmodulin kinase II delta) KO mice (n=3 hearts) showing loss of CaMKIIδ protein expression in CaMKIIδ-KO vs WT hearts (with GAPDH loading controls). D, WT or CaMKIIδ-KO cardiomyocytes were treated with 150 μM GSNO and paced at 0.5 Hz. There was no change in Ca²⁺ transient amplitude (E) or decay kinetics (F). In quiescent cardiomyocytes, Ca²⁺ sparks were measured from line-scan images (G), and there was also no effect of GSNO on Ca²⁺ spark frequency in either WT or CaMKIIδ-KO cardiomyocytes (H; WT: n=8 cells, N=3 hearts; CaMKIIδ-KO: n=8 cells, N=3 hearts).