Key result
Overexpression of human DDAH I in transgenic mice increased tissue NOS activity and reduced systolic blood pressure by 13 mm Hg compared to wild-type controls (P<0.05).
Population
Cultured endothelial cells in vitro and hDDAH-1 transgenic mice in vivo
Comparison
Overexpression of human DDAH I via gene transfer… vs Wild-type controls
Design
Preclinical
Authors
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Should not change practice; extends preclinical evidence linking DDAH I to BP regulation via ADMA-NOS.
p-value: p=<0.05
Overexpression of DDAH I increases nitric oxide synthesis by reducing endogenous ADMA levels, leading to decreased blood pressure and vascular resistance in a transgenic mouse model.
Dayoub et al. (2003) studied Cardiovascular physiology / NOS regulation. Overexpression of human DDAH I (hDDAH-1) vs. Wild-type controls was evaluated on NOS activity, NO production, and systolic blood pressure (p=<0.05). Overexpression of human DDAH I in transgenic mice increased tissue NOS activity and reduced systolic blood pressure by 13 mm Hg compared to wild-type controls (P<0.05).
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