Identification of a Cytochrome P450 2C9-Derived Endothelium-Derived Hyperpolarizing Factor in Essential Hypertensive Patients
Stefano Taddei, MD*,
Daniele Versari, MD,
Alessandro Cipriano, MD,
Lorenzo Ghiadoni, MD, PhD,
Fabio Galetta, MD,
Ferdinando Franzoni, MD,
Armando Magagna, MD,
Agostino Virdis, MD and
Antonio Salvetti, MD
Department of Internal Medicine, University of Pisa, Pisa, Italy
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Figure 2 Percent inhibition by sulfaphenazole on maximal response to acetylcholine (Ach) or bradykinin (Bdk) in normotensive subjects and essential hypertensive patients in control condition (saline) and under vitamin C. Data shown as mean ± SEM. *p < 0.001 versus other groups;  p < 0.05 versus Ach under saline in hypertensive patients (by analysis of variance and Scheffs test).
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Figure 3 Forearm blood flow (FBF) percent increase above basal induced by acetylcholine (n = 8) and bradykinin (n = 8) during saline, NG-monomethyl-L-arginine (L-NMMA), sulfaphenazole, and L-NMMA plus sulfaphenazole, in normotensive subjects. Data shown as mean ± SEM. *p < 0.001; p < 0.01 (by analysis of variance for repeated measures and Scheffé's test).
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Figure 4 Forearm blood flow (FBF) percent increase above basal induced by acetylcholine (upper panels) and bradykinin (lower panels) during saline or sulfaphenazole, at baseline (control) and under vitamin C in essential hypertensive patients. Data shown as mean ± SEM. *p < 0.05; p < 0.01 (by analysis of variance for repeated measures and Scheffé's test).
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p < 0.01 (by analysis of variance for repeated measures and Scheffé's test).