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Published on: October 15, 2010
Acute hyperhomocysteinaemia affects pulse pressure but not microvascular vasodilator function
1School of Medical and Surgical Sciences, University of Nottingham, UK.
British Journal of Clinical Pharmacology
|September 19, 2001
Summary
Acute hyperhomocysteinaemia increases pulse pressure, indicating larger vessel stiffness. However, it does not impact small vessel vasodilation responses, particularly non-nitric oxide pathways.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Metabolic Syndrome
Background:
- Elevated homocysteine (hcy) is linked to premature coronary artery disease.
- The precise vascular mechanisms, especially concerning small vessel vasodilation and non-nitric oxide (NO) pathways, remain unclear.
Purpose of the Study:
- To investigate the impact of acute hyperhomocysteinaemia on cutaneous microvascular vasodilator responses.
- To assess the effects on endothelial-dependent and independent vasodilation pathways.
- To evaluate changes in systemic haemodynamics and von Willebrand factor (vWF) levels.
Main Methods:
- A double-blind, placebo-controlled crossover study involving 14 healthy males.
- Acute hyperhomocysteinaemia was induced by oral methionine (15 g).
- Cutaneous microvascular vasodilation was measured using laser Doppler fluximetry (LDF) in response to acetylcholine (Ach) and sodium nitroprusside (SNP) iontophoresis.
Main Results:
- Methionine administration significantly elevated plasma hcy levels.
- A significant increase in pulse pressure was observed, suggesting increased large vessel stiffness.
- No significant changes were found in microvascular vasodilator responses to Ach or SNP, nor in vWF levels.
Conclusions:
- Acute hyperhomocysteinaemia increases pulse pressure, a marker of arterial stiffness.
- It does not impair endothelial-dependent (non-NO-mediated) microvascular vasodilation in healthy individuals.
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