FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2105456870> ?p ?o ?g. }

• W2105456870 endingPage "613" @default.
• W2105456870 startingPage "612" @default.
• W2105456870 abstract "HomeHypertensionVol. 55, No. 3Arterial Stiffness and Endothelial Function Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBArterial Stiffness and Endothelial FunctionKey Players in Vascular Health Daniel A. Duprez Daniel A. DuprezDaniel A. Duprez From the Cardiovascular Division, Medical School, University of Minnesota, Minneapolis, Minn. Search for more papers by this author Originally published18 Jan 2010https://doi.org/10.1161/HYPERTENSIONAHA.109.144725Hypertension. 2010;55:612–613Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 18, 2010: Previous Version 1 Functional assessment of the blood pressure waveform helps us to obtain an estimation of the arterial stiffness or its converse, arterial elasticity.1 Several epidemiological studies have clearly demonstrated that arterial stiffness is a significant predictor of cardiovascular disease incidence in the general population.2 There is clear evidence now that decreased arterial elasticity or increased arterial stiffness in normotensive and prehypertensive subjects induces increased risk for the development of arterial hypertension. In vitro and in vivo experiments have shown that the vascular endothelium plays a crucial role in vascular tone and consequently in arterial stiffness. However, there are no data available regarding the endothelial pathways involved in the adaptation of arterial mechanics during changes in blood flow.The elegant study by Bellien et al3 in this issue of Hypertension studied the endothelial pathways involved in the adaption of arterial mechanics during changes in blood flow. Besides identifying the “endothelial-derived relaxing factor” nitric oxide (NO) as important in this biological process, a unique aspect found in their study was the “endothelial-hyperpolarizing factor” EDHF. Endothelium-dependent relaxation/vasodilation in response to neurohumoral mediators and physical forces, such as the shear stress caused by blood flow, is generally attributed to the release of NO and/or prostacyclin. However, NO and prostacyclin cannot fully explain these endothelium-mediated vasodilator responses. The relaxations observed in the presence of NO synthase and cyclooxygenase inhibitors are often associated with hyperpolarization of the vascular smooth muscle cells and were first attributed to EDHF.4 The acronym “EDHF” turned out to be confusing because it seemed to imply that a single diffusible substance mediates this type of endothelium-dependent relaxation.5 In fact, in addition to NO itself, numerous endothelium-derived factors, including carbon monoxide, hydrogen sulfide, reactive oxygen species, peptides, and arachidonic acid metabolites derived from the cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase pathways can hyperpolarize the underlying smooth muscle cell.The nonlinear elastic response of arteries implies that their mechanical properties depend strongly on blood pressure. Thus, dynamic measurements of both the diameter and pressure curves over the whole cardiac cycle are necessary to characterize the arterial elastic behavior properly. In this study, the echotracking device NIUS02 was used to measure the cross-sectional compliance as a means of evaluating deformability of the arterial chamber, the incremental elastic modulus was used to evaluate the arterial stiffness and the midwall stress was calculated as means of evaluating the arterial wall loading conditions.6 This apparatus uses a radiofrequency signal and is sufficiently precise to determine change in arterial diameter as low as 1 μm across the cardiac cycle. It is possible to determine the pressure-diameter curve of the artery, thus to determine arterial stiffness for any given blood pressure. A major advantage of this methodology is that local arterial stiffness is directly determined from the change in pressure that drives the change in volume, ie, without using any model of the global circulation. This technique for measuring local arterial stiffness is not well known and is little used because it requires a high degree of technical expertise and takes longer to perform than do global techniques, such as measurement of pulse-wave velocity. Local measurement of arterial stiffness is largely indicated for mechanistic analyses in pathophysiology, pharmacology, and therapeutics and does not appear to be suited for epidemiological studies.The major findings of Bellien et al3 were that local inhibition of both NO and EDHF pathways in vivo in humans fully prevents the decrease in smooth muscle tone and wall stiffness of the radial artery during hand skin heating. These observations showed the major role of these endothelium-derived factors in the adaptation of peripheral conduit artery mechanics to changes in blood flow. Their results were the first demonstration of the role of a cytochrome-related EDHF in the adaptation of peripheral conduit artery mechanical properties to an increase in flow in humans. Beyond their human studies, Bellien et al3 studied the detailed mechanism of action of pharmacological inhibitors of the EDHF pathway using in vitro coronary vascular studies in wild-type FVB mice. This vascular model was chosen based on their previous experiments demonstrating the model is characterized by prominent NO-independent, EDHF-mediated relaxations.The endothelial cells are the interface between the blood and the vascular wall and are involved in many physiological functions in the cardiovascular system. They maintain the balance between vasodilation and vasoconstriction. In the past, EDHF was considered as a diffusible substance which mediated endothelium-dependent relaxation. However, NO and other endothelium-derived relaxing factors can hyperpolarize the underlying smooth muscle cells. Hyperpolarization decreases Ca2+ influx, by reducing the open probability of Cav channel-dependent activation of the sarcoplasmatic reticulum, which is a powerful means to produce the relaxation of vascular smooth muscle cells.7Another pathway for relaxing vascular smooth muscle cells does not involve the synthesis and the release of a factor. This pathway is associated with the hyperpolarization of both endothelial cells and vascular smooth muscle cells (EDHF-mediated responses) and also contributes to endothelium-dependent relaxations. These responses involve an increase in the intracellular Ca2+ concentration of endothelial cells and a subsequent hyperpolarization of these cells.8 Then, the underlying smooth muscle cells can be evoked by direct electric coupling through myoendothelial junctions and/or the accumulation of K+ ions in the intercellular space between the two cell types. The Figure illustrates these mechanisms in a simplified manner. Download figureDownload PowerPointFigure. Diagram depicting 2 pathways leading to vasodilation and reduced arterial stiffness. A, Hyperpolarization of the endothelial cell resulting from shear stress. B, Production of EDHF and NO induced by an agonist. Pathways A and B may occur simultaneously.The next step in this line of research is to translate these findings into clinical practice. It is generally accepted that atherosclerotic disease is associated with a decrease in NO synthesis and/or loss of its biological activities. Further research is necessary to explore whether alterations in the EDHF pathway also contributes to these endothelial dysfunctions or, conversely, compensates for the loss of NO bioavailability.Alterations of EDHF-mediated responses have been described with aging, hypertension, atherosclerosis, diabetes, hypercholesterolemia, and heart failure.9Some therapeutic interventions, such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, can restore the EDHF-mediated responses.10The improvement or restoration of EDHF responses has not yet been the focus of any pharmaceutical development effort. At this moment, there is an urgent need to further explore the importance of the endothelium-dependent hyperpolarization and to elaborate on electrophysiological measurements and pharmacological tools.It would be interesting also to study the effect of EDHF-mediated response on small versus large arteries beyond the effect of NO.In conclusion, since the discovery of NO as pioneer molecule in the endothelium-mediated regulation of vascular tone, the EDHF pathway has been revealed as an alternate mechanism for endothelial-mediated vascular control. Further research is necessary to understand the crosstalk between these 2 pathways with the ultimate aim to target therapy for maintaining vascular health.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.Sources of FundingNone.DisclosuresNone.FootnotesCorrespondence to Daniel A. Duprez, Cardiovascular Division, Medical School, University of Minnesota, 420 Delaware St SE, MMC 508, Minneapolis, MN 55455. E-mail [email protected] References 1 Cohn JN, Duprez DA, Finkelstein SM. Comprehensive noninvasive arterial vascular evaluation. Future Cardiol. 2009; 5: 573–579.CrossrefMedlineGoogle Scholar2 Duprez DA, Cohn JN. Arterial stiffness as a risk factor for coronary atherosclerosis. Curr Atheroscler Rep. 2007; 9: 139–144.CrossrefMedlineGoogle Scholar3 Bellien J, Favre J, Iacob M, Gao J, Thuillez C, Richard V, Joannidès R. Arterial stiffness is regulated by nitric oxide and endothelium-derived hyperpolarizing factor during changes in blood flow in humans. Hypertension. 2010; 55: 674–680.LinkGoogle Scholar4 Félétou M, Vanhoutte PM. EDHF: an update. Clin Sci (Lond). 2009; 117: 139–155.CrossrefMedlineGoogle Scholar5 Félétou M, Vanhoutte PM. Endothelium hyperpolarization: past beliefs and present facts. Ann Med. 2007; 39: 495–516.CrossrefMedlineGoogle Scholar6 Tardy Y, Meister JJ, Perret F, Brunner HR, Arditi M. Non-invasive estimate of the mechanical properties of peripheral arteries from ultrasonic and photoplethysmographic measurements. Clin Phys Physiol Meas. 1991; 12: 39–54.CrossrefMedlineGoogle Scholar7 Ledoux J, Werner ME, Brayden JE, Nelson MT. Calcium-activated potassium channels and the regulation of vascular tone. Physiology. 2006; 21: 69–78.CrossrefMedlineGoogle Scholar8 Emerson GG, Segal SS. Electrical coupling between endothelial cells and smooth muscle cells in hamster feed arteries: role in vasomotor control. Circ Res. 2000; 87: 474–479.CrossrefMedlineGoogle Scholar9 Selemidis S, Cocks TM. Endothelium-dependent hyperpolarization as a remote anti-atherogenic mechanism. Trends Pharmacol Sci. 2002; 23: 213–220.CrossrefMedlineGoogle Scholar10 Goto K, Fujii K, Onaka U, Abe I, Fujishima M. Renin-angiotensin system blockade improves endothelial dysfunction in hypertension. Hypertension. 2000; 36: 575–580.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Rahimi O, Melo A, Westwood B, Grier R, Tallant E and Gallagher P (2022) Angiotensin-(1-7) reduces doxorubicin-induced aortic arch dysfunction in male and female juvenile Sprague Dawley rats through pleiotropic mechanisms, Peptides, 10.1016/j.peptides.2022.170784, 152, (170784), Online publication date: 1-Jun-2022. Ji N, Huang Z, Zhang X, Sun Y, Ye S, Chen S, Tucker K, Wu S and Gao X (2021) Association between egg consumption and arterial stiffness: a longitudinal study, Nutrition Journal, 10.1186/s12937-021-00720-6, 20:1, Online publication date: 1-Dec-2021. Weinbaum S, Cancel L, Fu B and Tarbell J (2020) The Glycocalyx and Its Role in Vascular Physiology and Vascular Related Diseases, Cardiovascular Engineering and Technology, 10.1007/s13239-020-00485-9, 12:1, (37-71), Online publication date: 1-Feb-2021. Mahmoud M, Mayer M, Cancel L, Bartosch A, Mathews R and Tarbell J (2020) The glycocalyx core protein Glypican 1 protects vessel wall endothelial cells from stiffness-mediated dysfunction and disease, Cardiovascular Research, 10.1093/cvr/cvaa201, 117:6, (1592-1605), Online publication date: 25-May-2021. Amarasekera A, Chang D, Schwarz P and Tan T (2020) Does vascular endothelial dysfunction play a role in physical frailty and sarcopenia? A systematic review, Age and Ageing, 10.1093/ageing/afaa237, 50:3, (725-732), Online publication date: 5-May-2021. Dadayeva V, Fedorovich A, Mikhailova M, Kim O and Drapkina O (2020) The state of vascular wall in obesity, Profilakticheskaya meditsina, 10.17116/profmed202023051158, 23:5, (158), . Lamacchia O and Sorrentino M Diabetes Mellitus, Arterial Stiffness and Cardiovascular Disease: Clinical Implications and the Influence of SGLT2i, Current Vascular Pharmacology, 10.2174/1570161118666200317150359, 19:2, (233-240) Patil S, Biradar M, Khode V, Vadiraja H, Patil N and Raghavendra R (2020) Effectiveness of yoga on arterial stiffness: A systematic review, Complementary Therapies in Medicine, 10.1016/j.ctim.2020.102484, 52, (102484), Online publication date: 1-Aug-2020. Perissiou M, Bailey T, Windsor M, Leicht A, Golledge J and Askew C (2018) Reliability of arterial stiffness indices at rest and following a single bout of moderate-intensity exercise in older adults, Clinical Physiology and Functional Imaging, 10.1111/cpf.12537, 39:1, (42-50), Online publication date: 1-Jan-2019. Tomschi F, Köster P, Predel H, Lay D, Bloch W and Grau M (2018) Acute effects of lower and upper body-resistance training on arterial stiffness, peripheral, and central blood pressure in young normotensive women, Sport Sciences for Health, 10.1007/s11332-018-0440-7, 14:2, (357-363), Online publication date: 1-Aug-2018. Son W, Sung K, Cho J and Park S (2017) Combined exercise reduces arterial stiffness, blood pressure, and blood markers for cardiovascular risk in postmenopausal women with hypertension, Menopause, 10.1097/GME.0000000000000765, 24:3, (262-268), Online publication date: 1-Mar-2017. Palombo C and Kozakova M (2016) Arterial stiffness, atherosclerosis and cardiovascular risk: Pathophysiologic mechanisms and emerging clinical indications, Vascular Pharmacology, 10.1016/j.vph.2015.11.083, 77, (1-7), Online publication date: 1-Feb-2016. Gordin D and Groop P (2016) Aspects of Hyperglycemia Contribution to Arterial Stiffness and Cardiovascular Complications in Patients With Type 1 Diabetes, Journal of Diabetes Science and Technology, 10.1177/1932296816636894, 10:5, (1059-1064), Online publication date: 1-Sep-2016. Strohbach A and Busch R (2015) Polymers for Cardiovascular Stent Coatings, International Journal of Polymer Science, 10.1155/2015/782653, 2015, (1-11), . Lenders M, Hofschröer V, Schmitz B, Kasprzak B, Rohlmann A, Missler M, Pavenstädt H, Oberleithner H, Brand S, Kusche-Vihrog K and Brand E (2015) Differential response to endothelial epithelial sodium channel inhibition ex vivo correlates with arterial stiffness in humans, Journal of Hypertension, 10.1097/HJH.0000000000000736, 33:12, (2455-2462), Online publication date: 1-Dec-2015. Logan J, Engler M and Kim H (2014) Genetic Determinants of Arterial Stiffness, Journal of Cardiovascular Translational Research, 10.1007/s12265-014-9597-x, 8:1, (23-43), Online publication date: 1-Feb-2015. Sá da Fonseca L, Mota-Gomes M and Rabelo L (2014) Radial Applanation Tonometry as an Adjuvant Tool in the Noninvasive Arterial Stiffness and Blood Pressure Assessment, World Journal of Cardiovascular Diseases, 10.4236/wjcd.2014.45030, 04:05, (225-235), . Schmitz B, Brand S and Brand E (2014) Aldosterone signaling and soluble adenylyl cyclase—A nexus for the kidney and vascular endothelium, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 10.1016/j.bbadis.2014.05.036, 1842:12, (2601-2609), Online publication date: 1-Dec-2014. Triggle C, Samuel S, Ravishankar S, Marei I, Arunachalam G and Ding H (2012) The endothelium: influencing vascular smooth muscle in many ways, Canadian Journal of Physiology and Pharmacology, 10.1139/y2012-073, 90:6, (713-738), Online publication date: 1-Jun-2012. Wang J, Xu J, Zhou C, Zhang Y, Xu D, Guo Y and Yang Z (2012) Improvement of Arterial Stiffness by Reducing Oxidative Stress Damage in Elderly Hypertensive Patients After 6 Months of Atorvastatin Therapy, The Journal of Clinical Hypertension, 10.1111/j.1751-7176.2012.00600.x, 14:4, (245-249), Online publication date: 1-Apr-2012. Strohbach A, Begunk R, Petersen S, Felix S, Sternberg K and Busch R (2016) Biodegradable Polymers Influence the Effect of Atorvastatin on Human Coronary Artery Cells, International Journal of Molecular Sciences, 10.3390/ijms17020148, 17:2, (148) Mahmoud M, Cancel L and Tarbell J (2021) Matrix Stiffness Affects Glycocalyx Expression in Cultured Endothelial Cells, Frontiers in Cell and Developmental Biology, 10.3389/fcell.2021.731666, 9 Chen G, Zhao L, Feng J, You G, Sun Q, Li P, Han D, Zhou H and Lionetti V (2013) Validation of Reliable Reference Genes for Real-Time PCR in Human Umbilical Vein Endothelial Cells on Substrates with Different Stiffness, PLoS ONE, 10.1371/journal.pone.0067360, 8:6, (e67360) March 2010Vol 55, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.109.144725PMID: 20083729 Originally publishedJanuary 18, 2010 PDF download Advertisement SubjectsCalcium Cycling/Excitation-Contraction CouplingCoronary CirculationEndothelium/Vascular Type/Nitric OxideEtiologyIon Channels/Membrane TransportVascular Biology" @default.
• W2105456870 created "2016-06-24" @default.
• W2105456870 creator A5075267063 @default.
• W2105456870 date "2010-03-01" @default.
• W2105456870 modified "2023-09-25" @default.
• W2105456870 title "Arterial Stiffness and Endothelial Function" @default.
• W2105456870 cites W1967571831 @default.
• W2105456870 cites W1978654544 @default.
• W2105456870 cites W1978807721 @default.
• W2105456870 cites W1996502270 @default.
• W2105456870 cites W2017851551 @default.
• W2105456870 cites W2064489455 @default.
• W2105456870 cites W2127209378 @default.
• W2105456870 cites W2171552504 @default.
• W2105456870 doi "https://doi.org/10.1161/hypertensionaha.109.144725" @default.
• W2105456870 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20083729" @default.
• W2105456870 hasPublicationYear "2010" @default.
• W2105456870 type Work @default.
• W2105456870 sameAs 2105456870 @default.
• W2105456870 citedByCount "27" @default.
• W2105456870 countsByYear W21054568702012 @default.
• W2105456870 countsByYear W21054568702013 @default.
• W2105456870 countsByYear W21054568702014 @default.
• W2105456870 countsByYear W21054568702015 @default.
• W2105456870 countsByYear W21054568702016 @default.
• W2105456870 countsByYear W21054568702017 @default.
• W2105456870 countsByYear W21054568702018 @default.
• W2105456870 countsByYear W21054568702020 @default.
• W2105456870 countsByYear W21054568702021 @default.
• W2105456870 countsByYear W21054568702022 @default.
• W2105456870 countsByYear W21054568702023 @default.
• W2105456870 crossrefType "journal-article" @default.
• W2105456870 hasAuthorship W2105456870A5075267063 @default.
• W2105456870 hasConcept C126322002 @default.
• W2105456870 hasConcept C14036430 @default.
• W2105456870 hasConcept C164705383 @default.
• W2105456870 hasConcept C2775850156 @default.
• W2105456870 hasConcept C2776992346 @default.
• W2105456870 hasConcept C2780972559 @default.
• W2105456870 hasConcept C71924100 @default.
• W2105456870 hasConcept C84393581 @default.
• W2105456870 hasConcept C86803240 @default.
• W2105456870 hasConcept C95444343 @default.
• W2105456870 hasConceptScore W2105456870C126322002 @default.
• W2105456870 hasConceptScore W2105456870C14036430 @default.
• W2105456870 hasConceptScore W2105456870C164705383 @default.
• W2105456870 hasConceptScore W2105456870C2775850156 @default.
• W2105456870 hasConceptScore W2105456870C2776992346 @default.
• W2105456870 hasConceptScore W2105456870C2780972559 @default.
• W2105456870 hasConceptScore W2105456870C71924100 @default.
• W2105456870 hasConceptScore W2105456870C84393581 @default.
• W2105456870 hasConceptScore W2105456870C86803240 @default.
• W2105456870 hasConceptScore W2105456870C95444343 @default.
• W2105456870 hasIssue "3" @default.
• W2105456870 hasLocation W21054568701 @default.
• W2105456870 hasLocation W21054568702 @default.
• W2105456870 hasOpenAccess W2105456870 @default.
• W2105456870 hasPrimaryLocation W21054568701 @default.
• W2105456870 hasRelatedWork W2110375813 @default.
• W2105456870 hasRelatedWork W2125644036 @default.
• W2105456870 hasRelatedWork W2397330025 @default.
• W2105456870 hasRelatedWork W2410330942 @default.
• W2105456870 hasRelatedWork W2793577865 @default.
• W2105456870 hasRelatedWork W2996549374 @default.
• W2105456870 hasRelatedWork W3032402837 @default.
• W2105456870 hasRelatedWork W4205626535 @default.
• W2105456870 hasRelatedWork W4285164494 @default.
• W2105456870 hasRelatedWork W4313401325 @default.
• W2105456870 hasVolume "55" @default.
• W2105456870 isParatext "false" @default.
• W2105456870 isRetracted "false" @default.
• W2105456870 magId "2105456870" @default.
• W2105456870 workType "article" @default.