Trial reportVascular health and risk management2005
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral alpa1-adrenoceptor activation.
Trial report in Vascular health and risk management, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Cucurbitacins extracted from Cucumis melo L. (CuEC) exert a hypotensive effect via regulating vascular tone.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- CORP: Ultrasound assessment of vascular function with the passive leg movement technique.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe release of nitric oxide is controlled by cholinergic and adrenergic receptors. Recent observations suggest that activation of alpha-adrenoceptors can inhibit the release of nitric oxide. The aim of the present study was to examine the effect of alpha1- and alpha2-adrenoceptor activation on nitric oxide-mediated vasodilation. METHODOLOGY: In a first set of experiments, the endothelium-dependent vasodilators acetylcholine (ACh), 5-hydroxytryptamine (5HT), and bradykinin (BK), and the nitric oxide donor sodium nitroprusside (SNP) were administered in a random order in the brachial artery together with saline, or the nonselective alpha-adrenoceptor agonists norepinephrine or clonidine, or the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). The infusions of saline, norepinephrine, clonidine, and L-NMMA started 10 minutes before the infusions of ACh, BK, 5HT, and SNP. In a second set of experiments, cumulative doses of ACh, BK, and 5HT were infused, in a random order, intra-arterially together with saline or the selective alpha1-adrenoceptor agonist methoxamine. The infusions of saline and methoxamine started 5 minutes before the infusions of ACh, BK, and 5HT. Forearm blood flow was measured using computerized venous occlusion plethysmography.
resultsACh, 5HT, BK, and SNP induced a significant increase in forearm blood flow (p < 0.05 for all). These vasodilator responses were significantly attenuated by norepinephrine, clonidine, and L-NMMA (p <0.05 for all), except for SNP. In the second set of experiments, all three endothelium-dependent vasodilators induced a dose-dependent vasodilation, which was significantly inhibited by methoxamine (p <0.05).
conclusionThese results show that endothelium-dependent nitric oxide-mediated vasodilation is inhibited by activation of peripheral alpha1-adrenoceptors.
Indexed as
Identifiers
17319111PMC1993953What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.