Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity
IntroductionHypertension and impaired tissue perfusion are frequent comorbidities in obesity. Since resistance arteries are the primary regulators of peripheral resistance and hence, systemic blood pressure and local blood flow control, we hypothesized that resistance arteries isolated from obese mi...
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Frontiers Media S.A.
2025-08-01
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| author | Darcy Lidington Darcy Lidington Darcy Lidington Danny D. Dinh Danny D. Dinh Danny D. Dinh Nan Chen Nan Chen Hangjun Zhang Hangjun Zhang Yu-Qing Zhou Scott P. Heximer Scott P. Heximer Daniel A. Winer Daniel A. Winer Daniel A. Winer Daniel A. Winer Alexandre Martchenko Alexandre Martchenko Alexandre Martchenko Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz |
| author_facet | Darcy Lidington Darcy Lidington Darcy Lidington Danny D. Dinh Danny D. Dinh Danny D. Dinh Nan Chen Nan Chen Hangjun Zhang Hangjun Zhang Yu-Qing Zhou Scott P. Heximer Scott P. Heximer Daniel A. Winer Daniel A. Winer Daniel A. Winer Daniel A. Winer Alexandre Martchenko Alexandre Martchenko Alexandre Martchenko Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz |
| author_sort | Darcy Lidington |
| collection | DOAJ |
| description | IntroductionHypertension and impaired tissue perfusion are frequent comorbidities in obesity. Since resistance arteries are the primary regulators of peripheral resistance and hence, systemic blood pressure and local blood flow control, we hypothesized that resistance arteries isolated from obese mice would display augmented myogenic reactivity and altered vasomotor responses, compared to non-obese controls. MethodsEight-week-old C57BL/6J mice were fed either a high-fat diet (60% calories from fat; HFD) or a matched control diet for 16 weeks. Body weight, fasting blood glucose, oral glucose tolerance and insulin tolerance were measured. In parallel studies, we measured mean arterial pressure, conducted echocardiographic measurements of cardiac morphology and function and assessed skeletal muscle, mesenteric and cerebral resistance artery reactivity ex vivo with pressure myography. ResultsHFD mice exhibited substantial weight gain and metabolic dysfunction compared to controls. Left ventricular wall thickness and mass were increased in HFD mice, but no other morphological or functional cardiac parameters were different from controls. Blood pressure was modestly increased in HFD mice (from 81 to 87 mmHg; measured under anesthesia); however, contrary to our hypothesis, resistance arteries from HFD mice showed no overt microvascular phenotype in any microvascular bed tested (i.e., no differences in passive diameter, myogenic reactivity or vasomotor responses to phenylephrine or acetylcholine). ConclusionWe conclude that resistance artery function is unaltered in this diet-induced model of obesity with metabolic dysfunction. |
| format | Article |
| id | doaj-art-30e71feeaa094e66853b9b7f38b6a27b |
| institution | DOAJ |
| issn | 1664-042X |
| language | English |
| publishDate | 2025-08-01 |
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| series | Frontiers in Physiology |
| spelling | doaj-art-30e71feeaa094e66853b9b7f38b6a27b2025-08-20T03:02:30ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2025-08-011610.3389/fphys.2025.16021551602155Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesityDarcy Lidington0Darcy Lidington1Darcy Lidington2Danny D. Dinh3Danny D. Dinh4Danny D. Dinh5Nan Chen6Nan Chen7Hangjun Zhang8Hangjun Zhang9Yu-Qing Zhou10Scott P. Heximer11Scott P. Heximer12Daniel A. Winer13Daniel A. Winer14Daniel A. Winer15Daniel A. Winer16Alexandre Martchenko17Alexandre Martchenko18Alexandre Martchenko19Steffen-Sebastian Bolz20Steffen-Sebastian Bolz21Steffen-Sebastian Bolz22Steffen-Sebastian Bolz23Department of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaQanatpharma Ltd., Toronto, ON, CanadaDepartment of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaQanatpharma Ltd., Toronto, ON, CanadaDivision of Cellular and Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON, CanadaDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, CanadaDepartment of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaDepartment of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaDivision of Cellular and Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON, CanadaDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, CanadaBuck Institute for Research on Aging, Novato, CA, United StatesDepartment of Immunology, University of Toronto, Toronto, ON, CanadaDepartment of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaQanatpharma Ltd., Toronto, ON, CanadaDepartment of Physiology, University of Toronto, Toronto, ON, CanadaThe Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, ON, CanadaQanatpharma AG, Stans, SwitzerlandAphaia Pharma AG, Zug, SwitzerlandIntroductionHypertension and impaired tissue perfusion are frequent comorbidities in obesity. Since resistance arteries are the primary regulators of peripheral resistance and hence, systemic blood pressure and local blood flow control, we hypothesized that resistance arteries isolated from obese mice would display augmented myogenic reactivity and altered vasomotor responses, compared to non-obese controls. MethodsEight-week-old C57BL/6J mice were fed either a high-fat diet (60% calories from fat; HFD) or a matched control diet for 16 weeks. Body weight, fasting blood glucose, oral glucose tolerance and insulin tolerance were measured. In parallel studies, we measured mean arterial pressure, conducted echocardiographic measurements of cardiac morphology and function and assessed skeletal muscle, mesenteric and cerebral resistance artery reactivity ex vivo with pressure myography. ResultsHFD mice exhibited substantial weight gain and metabolic dysfunction compared to controls. Left ventricular wall thickness and mass were increased in HFD mice, but no other morphological or functional cardiac parameters were different from controls. Blood pressure was modestly increased in HFD mice (from 81 to 87 mmHg; measured under anesthesia); however, contrary to our hypothesis, resistance arteries from HFD mice showed no overt microvascular phenotype in any microvascular bed tested (i.e., no differences in passive diameter, myogenic reactivity or vasomotor responses to phenylephrine or acetylcholine). ConclusionWe conclude that resistance artery function is unaltered in this diet-induced model of obesity with metabolic dysfunction.https://www.frontiersin.org/articles/10.3389/fphys.2025.1602155/fullobesityinsulin resistancemyogenic activityresistance arteriesechocardiographyimpaired glucose tolerance (IGT) |
| spellingShingle | Darcy Lidington Darcy Lidington Darcy Lidington Danny D. Dinh Danny D. Dinh Danny D. Dinh Nan Chen Nan Chen Hangjun Zhang Hangjun Zhang Yu-Qing Zhou Scott P. Heximer Scott P. Heximer Daniel A. Winer Daniel A. Winer Daniel A. Winer Daniel A. Winer Alexandre Martchenko Alexandre Martchenko Alexandre Martchenko Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz Steffen-Sebastian Bolz Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity Frontiers in Physiology obesity insulin resistance myogenic activity resistance arteries echocardiography impaired glucose tolerance (IGT) |
| title | Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity |
| title_full | Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity |
| title_fullStr | Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity |
| title_full_unstemmed | Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity |
| title_short | Blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet-induced obesity |
| title_sort | blood pressure is elevated in the absence of resistance artery dysfunction in a mouse model of diet induced obesity |
| topic | obesity insulin resistance myogenic activity resistance arteries echocardiography impaired glucose tolerance (IGT) |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2025.1602155/full |
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