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- W2000728605 abstract "We tested the hypothesis that removing endocardial endothelium (EE) negatively impacts the force-frequency relationship (FFR) of ventricular myocardium and dissected the signaling that underlies this phenomenon. EE of rat trabeculae was selectively damaged by brief (<1 s) exposure to 0.1% Triton X-100. Force, intracellular Ca 2+ transient (iCa 2+ ), and activity of protein kinase A (PKA) and protein kinase C (PKC) were determined. In control muscles, force and iCa 2+ increased as the stimulation frequency increased in steps of 0.5 Hz up to 3.0 Hz. However, EE-denuded (EED) muscles exhibited a markedly blunted FFR. Neither isoproterenol (ISO; 0.1–5 nmol/l) nor endothelin-1 (ET-1; 10–100 nmol/l) alone restored the slope of FFR in EED muscles. Intriguingly, however, a positive FFR was restored in EED preparations by combining low concentrations of ISO (0.1 nmol/l) and ET-1 (20 nmol/l). In intact muscles, PKA and PKC activity increased proportionally with the increase in frequency. This effect was completely lost in EED muscles. Again, combining ISO and ET-1 fully restored the frequency-dependent rise in PKA and PKC activity in EED muscles. In conclusion, selective damage of EE leads to significantly blunted FFR. A combination of low concentrations of ISO and ET-1 successfully restores FFR in EED muscles. The interdependence of ISO and ET-1 in this process indicates cross-talk between the β 1 -PKA and ET-1-PKC pathways for a normal (positive) FFR. The results also imply that dysfunction of EE and/or EE-myocyte coupling may contribute to flat (or even negative) FFR in heart failure." @default.
- W2000728605 created "2016-06-24" @default.
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- W2000728605 date "2013-08-01" @default.
- W2000728605 modified "2023-10-17" @default.
- W2000728605 title "Endocardial endothelium is a key determinant of force-frequency relationship in rat ventricular myocardium" @default.
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- W2000728605 doi "https://doi.org/10.1152/japplphysiol.01415.2012" @default.
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