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. 2023 Nov 14;133(12):1040–1055. doi: 10.1161/CIRCRESAHA.123.323571

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© 2023 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — Pretreatment with clinical NO donor sodium nitroprusside (SNP) and sGC (soluble guanylyl cyclase) inhibitor elicits similar protection against isoproterenol-induced Ca²⁺ sparks. Ca²⁺ transients (A) and sparks (B) from wild-type (WT) and CaMKIIδ (Ca²⁺/calmodulin kinase II delta)-C273S cardiomyocyte were recorded at the end of a 7-minute incubation with SNP (200 μM) followed by wash-in of 100 nmol/L ISO. Mean Ca²⁺ transient amplitude and spark frequency data are shown in C and D, respectively (WT: n=10 cells, N=3 hearts; CaMKIIδ-C273S: n=23 cells, N=6 hearts). The same experiments were performed following a pretreatment with sGC inhibitor ODQ (10 μM; 20 minutes incubation) with representative line-scans (E and F) and mean data (G and H) plotted for WT (n=13 cells, N=3 hearts) and CaMKIIδ-C273S (n=14 cells, N=4 hearts) cardiomyocytes. ISO indicates isoproterenol.