Effects of acute methionine loading and vitamin C on endogenous fibrinolysis, endothelium-dependent vasomotion and platelet aggregation

Clin Sci (Lond). 2001 Feb;100(2):127-35.

Abstract

We assessed forearm blood flow and plasma fibrinolytic factors in eight healthy males who received unilateral brachial artery infusions of the endothelium-dependent vasodilator, substance P, and the endothelium-independent vasodilator, sodium nitroprusside. These measurements, together with platelet aggregation studies, were performed on four occasions after double-blind randomized ingestion of placebo, methionine (0.1 mg/kg), vitamin C (2 g) and methionine plus vitamin C. Blood flow and platelet aggregation responses were unaffected by methionine loading. Substance P caused dose-dependent increases in plasma tissue plasminogen activator (t-PA) antigen (from 3.0+/-0.1 to 4.7+/-0.4 ng/ml; P<0.001) and activity (from 1.2+/-0.2 to 4.2+/-0.4 i.u./ml; P<0.001), which were augmented during acute methionine loading (4.7+/-0.4 to 5.6+/-0.5 ng/ml and 4.2+/-0.4 to 5.5+/-0.9 i.u./ml respectively; P</=0.05). Moreover, the estimated net release of t-PA was enhanced during methionine loading (two-way ANOVA; P=0.02), but this was unaffected by vitamin C supplementation. We conclude that, in the absence of alterations in endothelium-dependent vasomotion or platelet aggregation, substance P-induced t-PA release is enhanced following methionine loading. This suggests that the acute endogenous fibrinolytic capacity is augmented during acute hyperhomocysteinaemia in healthy humans via an oxidation-independent mechanism.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adult
  • Ascorbic Acid / pharmacology*
  • Dose-Response Relationship, Drug
  • Double-Blind Method
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / physiopathology
  • Fibrinolysis / drug effects*
  • Fibrinolysis / physiology
  • Forearm / blood supply
  • Humans
  • Hyperhomocysteinemia / blood*
  • Hyperhomocysteinemia / chemically induced
  • Hyperhomocysteinemia / physiopathology
  • Male
  • Methionine
  • Nitroprusside / pharmacology
  • Platelet Aggregation / drug effects*
  • Platelet Aggregation / physiology
  • Regional Blood Flow / drug effects
  • Substance P / pharmacology
  • Tissue Plasminogen Activator / blood
  • Vasodilation / drug effects
  • Vasodilation / physiology
  • Vasodilator Agents / pharmacology

Substances

  • Vasodilator Agents
  • Nitroprusside
  • Substance P
  • Methionine
  • Tissue Plasminogen Activator
  • Ascorbic Acid