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Abstract
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.
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.
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.