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. 2020 May 25;11:345. doi: 10.3389/fphys.2020.00345

FIGURE 1.

FIGURE 1

Cardiomyocyte passive stiffness and protein kinase (PK)G and PKA activity in the rat model. (A) Original recording of the force response to stepwise cell stretching of isolated skinned cardiomyocytes. (B) Control and Dahl salt-sensitive (DSS) passive force (Fpassive) at sarcomere length (SL) 1.8–2.4 μm in the presence or absence of in vivo soluble guanylyl cyclase (sGC) activator. (C,D) Control and DSS Fpassive at SL 1.8–2.4 μm in the presence or absence of in vivo sGC activator and subsequently added PKG. (E,F) Control and DSS Fpassive at SL 1.8–2.4 μm in the presence or absence of in vivo sGC activator and subsequently added PKG. Curves are second-order polynomial fits to the means (± SEM; n = 4–5 cardiomyocytes/heart). For (B), *P < 0.05 control baseline versus DSS baseline, †P < 0.05 DSS baseline versus DSS after sGC activator treatment. (D) *P < 0.05 DSS baseline versus DSS after sGC activator treatment, †P < 0.05 DSS after sGC activator treatment versus DSS after sGC activator treatment followed by PKG treatment. (F) *P < 0.05 DSS baseline versus DSS after sGC activator treatment followed by PKA in Student’s t-test. (G) PKG activity. (H) PKA activity. Data are shown as mean ± SEM; n = 7–8 left ventricular (LV) samples/group. *P < 0.05 control untreated versus DSS untreated and †P < 0.05 before versus after sGC activator treatment.