Glucocorticoid stimulation increases cardiac contractility by SGK1-dependent SOCE-activation in rat cardiac myocytes
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Key result
Dexamethasone pretreatment significantly increased developed left ventricular pressure from 107 to 148 mmHg in Langendorff-perfused rat hearts via a SOCE-dependent mechanism.
Why the study?
Glucocorticoid stimulation increases cardiac contractility through elevated intracellular calcium, but the sources for calcium entry remain unclear.
Population
Langendorff-perfused Sprague-Dawley rat hearts and isolated rat ventricular myocytes
Comparison
Dexamethasone pretreatment with or without SOCE or SGK1 inhibitors vs untreated controls
Design
Preclinical ex vivo and in vitro laboratory study
Authors
Discussion
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Implication
SOCE mediates glucocorticoid inotropy in rat hearts; hypothesis-generating and should not yet inform clinical practice.
Structured PICO
P
Population
Male Sprague-Dawley rats at 20 weeks of age were used to investigate the effects of dexamethasone on cardiac contractility.
I
Intervention
Dexamethasone (Dex) pretreatment (2 mg/kg BW i.p. 24 h prior to experiment for hearts; 1 mg/mL Dex for 24 h for isolated myocytes)
C
Comparator
Untreated hearts/myocytes
O
Outcome
Cardiac contractile force, Ca transient amplitude, and fractional shorteningsurrogate
Main Result
Absolute Event Rate: 148% vs 107%
p-value: p=0.0093
Short-term glucocorticoid stimulation with dexamethasone improves cardiac contractility via a SOCE-dependent mechanism involving SGK1-dependent expression of SOCE-related proteins.
Limitations
- The detailed route through which Ca enters the SR via SOCE needs to be further elucidated.
- Potential application of GC stimulation could interfere with the cellular stress response leading to disturbed Ca handling and arrhythmias.
Cite This Study
Wester et al. (2019) studied Healthy. Dexamethasone vs. Vehicle was evaluated on Developed left ventricular (systolic) pressure (LVP amplitude) (p=0.0093). Dexamethasone pretreatment significantly increased developed left ventricular pressure from 107 to 148 mmHg in Langendorff-perfused rat hearts via a SOCE-dependent mechanism.
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