Document Detail

Vitamin C improves endothelium-dependent vasodilation by restoring nitric oxide activity in essential hypertension.
MedLine Citation:
PMID:  9631871     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Essential hypertension is associated with impaired endothelium-dependent vasodilation. Inactivation of endothelium-derived nitric oxide by oxygen free radicals participates in endothelial dysfunction in experimental hypertension. To test this hypothesis in humans, we evaluated the effect of antioxidant vitamin C on endothelium-dependent responses in essential hypertensive patients. METHODS AND RESULTS: In 14 healthy subjects (47.1+/-4.8 years; blood pressure, 120.6+/-4.5/80.9+/-3.5 mm Hg) and 14 essential hypertensive patients (47.3+/-5.1 years; blood pressure, 153.9+/-7.1/102.3+/-4.1 mm Hg), we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 microg x 100 mL(-1) x min(-1)) or sodium nitroprusside (1, 2, and 4 microg/100 mL forearm tissue per minute), an endothelium-dependent and -independent vasodilator, respectively, in basal conditions and during infusion of intrabrachial vitamin C (2.4 mg/100 mL forearm tissue per minute). In hypertensive patients but not in control subjects, vitamin C increased (P<0.01) the impaired vasodilation to acetylcholine, whereas the response to sodium nitroprusside was unaffected. Moreover, in another 14 hypertensive patients (47.1+/-5.2 years; blood pressure, 155.2+/-6.9/103.7+/-4.5 mm Hg), the facilitating effect of vitamin C on vasodilation to acetylcholine was reversed by N(G)-monomethyl-L-arginine (100 microg/100 mL forearm tissue per minute), a nitric oxide synthase inhibitor, suggesting that in essential hypertension superoxide anions impair endothelium-dependent vasodilation by nitric oxide breakdown. Finally, because in adjunctive 7 hypertensive patients (47.8+/-6.1 years; blood pressure, 155.3+/-6.8/103.5+/-4.3 mm Hg), indomethacin (50 microg/100 mL forearm tissue per minute), a cyclooxygenase inhibitor, prevented the potentiating effect of vitamin C on vasodilation to acetylcholine, it is possible that in essential hypertension a main source of superoxide anions could be the cyclooxygenase pathway. CONCLUSIONS: In essential hypertensive patients, impaired endothelial vasodilation can be improved by the antioxidant vitamin C, an effect that can be reversed by the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine. These findings support the hypothesis that nitric oxide inactivation by oxygen free radicals contributes to endothelial dysfunction in essential hypertension.
S Taddei; A Virdis; L Ghiadoni; A Magagna; A Salvetti
Publication Detail:
Type:  Clinical Trial; Journal Article    
Journal Detail:
Title:  Circulation     Volume:  97     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1998 Jun 
Date Detail:
Created Date:  1998-07-09     Completed Date:  1998-07-09     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2222-9     Citation Subset:  AIM; IM    
I Clinica Medica, University of Pisa, Italy.
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MeSH Terms
Acetylcholine / pharmacology
Antioxidants / pharmacology*
Ascorbic Acid / pharmacology*
Cyclooxygenase Inhibitors / pharmacology
Dose-Response Relationship, Drug
Endothelium, Vascular / physiopathology*
Enzyme Inhibitors / pharmacology
Hypertension / physiopathology*
Indomethacin / pharmacology
Middle Aged
Nitric Oxide / metabolism*
Vasodilation / drug effects*
omega-N-Methylarginine / pharmacology
Reg. No./Substance:
0/Antioxidants; 0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 50-81-7/Ascorbic Acid; 51-84-3/Acetylcholine; 53-86-1/Indomethacin

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