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Acute hyperhomocysteinaemia affects pulse pressure but not microvascular vasodilator function
Author(s) -
Davis Karl R.,
Pearson Helen,
Moat Stuart,
Bonham James R.,
Donnelly Richard
Publication year - 2001
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.0306-5251.2001.01447.x
Subject(s) - sodium nitroprusside , vasodilation , medicine , nitric oxide , homocysteine , crossover study , blood pressure , cardiology , arterial stiffness , hemodynamics , endothelial dysfunction , placebo , pathology , alternative medicine
Aims Raised homocysteine (hcy) levels are associated with premature coronary artery disease, but the underlying vascular mechanism and the extent to which hcy affects small vessel vasodilator responses (especially non‐nitric oxide mediated pathways) are unclear. Methods This double‐blind, placebo‐controlled crossover study in 14 healthy male subjects evaluated the effects of single‐dose oral methionine 15 g (to induce acute hyperhomocysteinaemia) on cutaneous microvascular vasodilator responses to incremental‐dose iontophoretic administration of acetylcholine (Ach) and sodium nitroprusside (SNP) using laser Doppler fluximetry (LDF), and the effects on von Willibrand factor (vWF) levels and systemic haemodynamics. Results Methionine administration produced a three fold rise in plasma hcy levels at 8 h, which was accompanied by a significant increase in pulse pressure (53 vs 49 mmHg, P < 0.05) but no change in heart rate. Acute hyperhomocysteinaemia had no significant effect on incremental microvascular vasodilator dose–response curves to Ach and SNP, or circulating levels of vWF. Conclusions The present study shows that acute hyperhomocysteinaemia increases pulse pressure (a marker of large vessel stiffness) but has no effect on endothelial‐dependent (non‐NO‐mediated) microvascular vasodilation.