Linked Life Data

11244022

Source:http://linkedlifedata.com/resource/pubmed/id/11244022

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-3-13
pubmed:abstractText
Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Because calcium antagonists can improve endothelial function in patients with essential hypertension, in this study we tested the hypothesis that this beneficial effect could be related to restoration of NO availability by antioxidant properties. In 15 healthy subjects and 15 hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (ACh; 0.15, 0.45, 1.5, 4.5, and 15 microg/100 mL per minute), an endothelium-dependent vasodilator in basal conditions, during infusion of N:(G)-monomethyl-L-arginine (L-NMMA, 100 microg/100 mL forearm tissue per minute), an NO-synthase inhibitor, vitamin C (8 mg/100 mL forearm tissue per minute), and finally, simultaneous infusion of L-NMMA and vitamin C. The response to sodium nitroprusside (SNP; 1, 2, and 4 microg/100 mL forearm tissue per minute) was also evaluated. In control subjects, vasodilation to ACh was inhibited by L-NMMA and not changed by vitamin C. In hypertensive patients, vasodilation to ACh was blunted as compared with control subjects and resistant to L-NMMA. Vitamin C, which decreased plasma isoprostanes and increased plasma antioxidant capacity, increased the response to ACh and restored the inhibiting effect of L-NMMA. In hypertensive patients, the study was repeated after 3-month treatment with nifedipine gastrointestinal therapeutic system (30 to 60 mg/daily). Nifedipine treatment decreased circulating plasma lipoperoxides and isoprostanes and increased plasma antioxidant capacity. Moreover, nifedipine increased the vasodilation to ACh but not to SNP and restored the inhibiting effect of L-NMMA on ACh-induced vasodilation, whereas vitamin C no longer exerted its facilitating activity. These results indicate that nifedipine increases endothelium-dependent vasodilation by restoring NO availability, an effect probably determined by antioxidant activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
943-8
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:11244022-Acetylcholine, pubmed-meshheading:11244022-Antioxidants, pubmed-meshheading:11244022-Ascorbic Acid, pubmed-meshheading:11244022-Blood Pressure, pubmed-meshheading:11244022-Calcium Channel Blockers, pubmed-meshheading:11244022-Endothelium, Vascular, pubmed-meshheading:11244022-Enzyme Inhibitors, pubmed-meshheading:11244022-Female, pubmed-meshheading:11244022-Forearm, pubmed-meshheading:11244022-Heart Rate, pubmed-meshheading:11244022-Humans, pubmed-meshheading:11244022-Hypertension, pubmed-meshheading:11244022-Male, pubmed-meshheading:11244022-Middle Aged, pubmed-meshheading:11244022-Nifedipine, pubmed-meshheading:11244022-Nitric Oxide, pubmed-meshheading:11244022-Nitric Oxide Synthase, pubmed-meshheading:11244022-Oxidative Stress, pubmed-meshheading:11244022-Regional Blood Flow, pubmed-meshheading:11244022-Time Factors, pubmed-meshheading:11244022-Vasodilation, pubmed-meshheading:11244022-omega-N-Methylarginine
pubmed:year
2001
pubmed:articleTitle
Restoration of nitric oxide availability after calcium antagonist treatment in essential hypertension.
pubmed:affiliation
Department of Internal Medicine, University of Pisa (Italy). s.taddei@int.med.unipi.it
pubmed:publicationType
Journal Article