Key result
Endothelial eNOS overexpression doubles bradykinin-induced reduction in myocardial oxygen consumption in mice.
Why the study?
The role of selective endothelial nitric oxide synthase (eNOS) overexpression in coronary vessels in controlling myocardial oxygen consumption was unclear.
Population
22 transgenic eNOS-overexpressing mice and 24 wild-type mice
Comparison
eNOS-overexpressing mice vs wild-type mice
Design
Preclinical experimental study in mice
Authors
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Vascular eNOS may modulate myocardial energetics; animal data extend mechanistic insights but leave clinical translation open.
Absolute Event Rate: 33% vs 17%
p-value: p=<0.05
Selective overexpression of eNOS in cardiac blood vessels in mice enhances the control of myocardial oxygen consumption by eNOS-derived NO.
Walsh et al. (2004) studied this question. Selective endothelial nitric oxide synthase (eNOS) overexpression vs. Wild-type mice was evaluated on Percent decrease in myocardial oxygen consumption (MVO2) in response to bradykinin (10^-4 mol/l) (p=<0.05). Selective overexpression of eNOS in cardiac blood vessels in mice significantly enhanced the reduction of myocardial oxygen consumption in response to bradykinin compared to wild-type mice (33% vs 17%, P<0.05).
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