Acute hyperhomocysteinaemia affects pulse pressure but not microvascular vasodilator function

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.