November 1, 2001Hypertension
Endothelium-Derived Nitric Oxide Regulates Arterial Elasticity in Human Arteries In Vivo
Key result
Inhibition of basal NO production by L-NMMA decreased brachial artery compliance (P<0.0001) and increased pulse wave velocity (P<0.0001), demonstrating NO augments arterial elasticity.
Why the study?
Does endothelium-derived NO regulate arterial elasticity in healthy young men?
Population
7 healthy young men
Comparison
N-monomethyl-L-arginine followed by nitroglycerin vs Baseline control conditions
Design
Other
Authors
Discussion
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Member takes
Implication
Endothelial NO supports brachial artery elasticity in healthy men; leaves open its role in disease or as therapeutic target.
Structured PICO
Does endothelium-derived NO regulate arterial elasticity in healthy young men?
P
Population
7 healthy young men
I
Intervention
N(G)-monomethyl-L-arginine (L-NMMA) (4 and 8 mg/min) followed by nitroglycerin (2.5 and 12.5 microgram/min)
C
Comparator
Baseline control conditions
O
Outcome
Indices of arterial elasticity (pressure-area relationship, instantaneous compliance, stress-strain, pressure-incremental elastic modulus, and pressure-pulse wave velocity relationships)surrogate
Main Result
p-value: p=<0.0001
Endothelium-derived NO constitutively regulates and augments arterial elasticity in the human brachial artery in vivo.
Cite This Study
Kinlay et al. (2001) studied Healthy (n=7). L-NMMA and Nitroglycerin vs. Baseline control was evaluated on Indices of arterial elasticity (brachial artery area, compliance, E(inc), and pulse wave velocity) (p=<0.0001). Inhibition of basal NO production by L-NMMA decreased brachial artery compliance (P<0.0001) and increased pulse wave velocity (P<0.0001), demonstrating NO augments arterial elasticity.