Key result
In endocardial cells from spontaneous hypertensive rats, the time required to reach peak K(ATP) channel currents was significantly longer compared to normal rats (319 vs 177 s, P=0.01).
Population
Endocardial and epicardial myocytes isolated from hypertrophied left ventricles of spontaneous hypertensive…
Comparison
Metabolic stress induced by 2 mM CN and no… vs Myocytes from normal Wistar-Kyoto rats (WKY)
Design
Preclinical
Authors
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Impaired endocardial K(ATP) activation may heighten ischemic vulnerability in hypertension; hypothesis-generating and requires human confirmation.
Absolute Event Rate: 319% vs 177%
p-value: p=0.01
K(ATP) channel activation under metabolic stress is impaired in endocardial cells from hypertrophied left ventricles, potentially contributing to maladaptive responses to ischemia.
Shimokawa et al. (2007) studied Left ventricular hypertrophy (n=46). Left ventricular hypertrophy (SHR) vs. Normal left ventricle (WKY) was evaluated on Time required to reach peak currents after onset of K(ATP) channel opening in endocardial cells (p=0.01). In endocardial cells from spontaneous hypertensive rats, the time required to reach peak K(ATP) channel currents was significantly longer compared to normal rats (319 vs 177 s, P=0.01).
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