Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation
Adriaan M Kamper, Anton JM de Craen, Rudi GJ Westendorp, Gerard J BlauwDepartments of Gerontology & Geriatrics, Leiden University Medical Center, Leiden, The NetherlandsObjectives: The release of nitric oxide is controlled by cholinergic and adrenergic receptors. Recent observations suggest...
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2005-10-01
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doaj-f01f560d83a4446c909be29766b7deb52020-11-24T20:41:29ZengDove Medical PressVascular Health and Risk Management1178-20482005-10-01Volume 12512561384Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activationAdriaan M KamperAnton JM de CraenRudi GJ WestendorpGerard J BlauwAdriaan M Kamper, Anton JM de Craen, Rudi GJ Westendorp, Gerard J BlauwDepartments of Gerontology & Geriatrics, Leiden University Medical Center, Leiden, The NetherlandsObjectives: The release of nitric oxide is controlled by cholinergic and adrenergic receptors. Recent observations suggest that activation of α-adrenoceptors can inhibit the release of nitric oxide. The aim of the present study was to examine the effect of α1- and α2-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 α-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 α1-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.Results: ACh, 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).Conclusion: These results show that endothelium-dependent nitric oxide-mediated vasodilation is inhibited by activation of peripheral α1-adrenoceptors.Keywords: acetylcholine, α-adrenoceptors, bradykinin, 5-hydroxytryptamine, nitric oxide, strain-gauge plethysmographyhttps://www.dovepress.com/endothelium-dependent-no-mediated-vasodilation-in-humans-is-attenuated-peer-reviewed-article-VHRM |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Adriaan M Kamper Anton JM de Craen Rudi GJ Westendorp Gerard J Blauw |
spellingShingle |
Adriaan M Kamper Anton JM de Craen Rudi GJ Westendorp Gerard J Blauw Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation Vascular Health and Risk Management |
author_facet |
Adriaan M Kamper Anton JM de Craen Rudi GJ Westendorp Gerard J Blauw |
author_sort |
Adriaan M Kamper |
title |
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
title_short |
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
title_full |
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
title_fullStr |
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
title_full_unstemmed |
Endothelium-dependent NO-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
title_sort |
endothelium-dependent no-mediated vasodilation in humans is attenuated by peripheral a1-adrenoceptor activation |
publisher |
Dove Medical Press |
series |
Vascular Health and Risk Management |
issn |
1178-2048 |
publishDate |
2005-10-01 |
description |
Adriaan M Kamper, Anton JM de Craen, Rudi GJ Westendorp, Gerard J BlauwDepartments of Gerontology & Geriatrics, Leiden University Medical Center, Leiden, The NetherlandsObjectives: The release of nitric oxide is controlled by cholinergic and adrenergic receptors. Recent observations suggest that activation of α-adrenoceptors can inhibit the release of nitric oxide. The aim of the present study was to examine the effect of α1- and α2-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 α-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 α1-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.Results: ACh, 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).Conclusion: These results show that endothelium-dependent nitric oxide-mediated vasodilation is inhibited by activation of peripheral α1-adrenoceptors.Keywords: acetylcholine, α-adrenoceptors, bradykinin, 5-hydroxytryptamine, nitric oxide, strain-gauge plethysmography |
url |
https://www.dovepress.com/endothelium-dependent-no-mediated-vasodilation-in-humans-is-attenuated-peer-reviewed-article-VHRM |
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