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Nifedipine inhibits superoxide production induced by pulsatile stretch in human aortic endothelial cells


Cosentino, F (2000). Nifedipine inhibits superoxide production induced by pulsatile stretch in human aortic endothelial cells. American Journal of Hypertension, 13(6):S34.

Abstract

Dihydropiridine calcium channel blocker nifedipine restores nitric oxide-mediated vasodilation in human hypertension. The mechanims involved have not been fully characterized but may relate to endothelial protection. Mechanical forces such as pulsatile stretch are involved in superoxide anion production. To clarify the effect of nifedipine on the balance between nitric oxide and superoxide anion, human cultured aortic endothelial cells were exposed to pulsatile stretch in the presence and in the absence of this compound. Rhytmic stretching was given for 1 hour by a computerized Flexercell strain unit (10% average elongation, 50 cycles per minute). Superoxide anion production was measured as the superoxide dismutase-inhibitable reduction of cytochrome c. Stretch-induced production of superoxide anion was inhibited in a concentration-dependent manner by nifedipine [6.2±0.9 vs 2.1±0.6* and 4.8±0.4*, 2.4±0.5* nmol/60 min/105 cells for stretch vs control and stetch plus nifedipine (10−7 and 10−6 M), respectively; n=6; *P<0.05 vs stretch]. This antioxidant activity of nifedipine may exert vascular protective effects in human endothelial cells. Thus, nifedipine may affect mechanical forces which, as determinants of the balance between nitric oxide and superoxide anion, are likely to play a key role in the pathophysiology of hypertensive vascular disease

Abstract

Dihydropiridine calcium channel blocker nifedipine restores nitric oxide-mediated vasodilation in human hypertension. The mechanims involved have not been fully characterized but may relate to endothelial protection. Mechanical forces such as pulsatile stretch are involved in superoxide anion production. To clarify the effect of nifedipine on the balance between nitric oxide and superoxide anion, human cultured aortic endothelial cells were exposed to pulsatile stretch in the presence and in the absence of this compound. Rhytmic stretching was given for 1 hour by a computerized Flexercell strain unit (10% average elongation, 50 cycles per minute). Superoxide anion production was measured as the superoxide dismutase-inhibitable reduction of cytochrome c. Stretch-induced production of superoxide anion was inhibited in a concentration-dependent manner by nifedipine [6.2±0.9 vs 2.1±0.6* and 4.8±0.4*, 2.4±0.5* nmol/60 min/105 cells for stretch vs control and stetch plus nifedipine (10−7 and 10−6 M), respectively; n=6; *P<0.05 vs stretch]. This antioxidant activity of nifedipine may exert vascular protective effects in human endothelial cells. Thus, nifedipine may affect mechanical forces which, as determinants of the balance between nitric oxide and superoxide anion, are likely to play a key role in the pathophysiology of hypertensive vascular disease

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:150 Psychology
Language:English
Date:1 June 2000
Deposited On:20 Sep 2018 14:00
Last Modified:17 Sep 2019 19:28
Publisher:Nature Publishing Group
ISSN:0895-7061
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/s0895-7061(00)00381-2
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101016S0895706100003812 (Library Catalogue)

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