Mechanisms responsible for endothelial dysfunction induced by fasting hyperhomocystinemia in normotensive subjects and patients with essential hypertension
Agostino Virdis, MDa,
Lorenzo Ghiadoni, MD, PhDa,
Heloise Cardinal, MDa,
Stefania Favilla, PhDa,
Piero Duranti, BSa,
Renzo Birindelli, BSa,
Armando Magagna, MDa,
Gianpaolo Bernini, MDa,
Guido Salvetti, MDa,
Stefano Taddei, MDa and
Antonio Salvetti, MDa
a Department of Internal Medicine, University of Pisa, Pisa, Italy
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Figure 1 Acetylcholine- and sodium nitroprusside (SNP)-induced increases in forearm blood flow (FBF) in normotensive subjects (top) and patients with essential hypertension (bottom), classified into those with normohomocystinemia (N-HCY; open circles) and hyperhomocystinemia (H-HCY; solid circles).
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Figure 2 Scatterplot of relationship between homocysteine (x axis) and maximal forearm blood flow response to acetylcholine (Ach; y axis) in normotensive subjects (top) and patients with essential hypertension (bottom). VD = vasodilation.
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Figure 3 Acetylcholine-induced increase in forearm blood flow (FBF) during saline (open circles) or NG-monomethyl-L-arginine (L-NMMA) (solid circles), in the absence (control) and presence of vitamin C in normohomocystinemic (N-HCY) and hyperhomocystinemic (H-HCY) normotensive subjects.
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Figure 4 Acetylcholine-induced increase in forearm blood flow (FBF) during saline (open circles) or NG-monomethyl-L-arginine (L-NMMA) (solid circles), in the absence (control) and presence of vitamin C in normohomocystinemic (N-HCY) and hyperhomocystinemic (H-HCY) patients with essential hypertension.
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