Intrinsic exercise capacity induces divergent vascular plasticity via arachidonic acid-mediated inflammatory pathways in female rats.
Test
Journal
Vascular pharmacology
ISSN: 1879-3649
Titre abrégé: Vascul Pharmacol
Pays: United States
ID NLM: 101130615
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
03
12
2020
revised:
03
03
2021
accepted:
07
04
2021
pubmed:
20
4
2021
medline:
26
3
2022
entrez:
19
4
2021
Statut:
ppublish
Résumé
Metabolic syndrome prevalence has increased among US adults, particularly among non-hispanic white and black women. Sedentary behavior often leads to chronic inflammation, a triggering factor of metabolic syndrome. Given that intrinsic exercise capacity is genetically inherited, we questioned if low-grade chronic inflammation would be present in a female rat model of low intrinsic exercise capacity-induced metabolic syndrome, while beneficial increase of resolution of inflammation would be present in a female rat model of high intrinsic exercise capacity. In the vascular system, two primary markers for inflammation and resolution of inflammation are cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Our study focused on the novel hypothesis that untrained, inherited exercise capacity induces divergent vascular plasticity via changes in the delicate balance between COX and LOX inflammatory mediators. We used divergent rat strains with low (LCR) and high (HCR) aerobic running capacity. By using animals with contrasting intrinsic exercise capacities, it is possible to determine the exact triggers that lead to inherited vascular plasticity in female rats. We observed that female LCR displayed increased periovarian fat pad and body weight, which is congruent with their obesity-presenting phenotype. Furthermore, LCR presented with vascular hypocontractility and increased COX and LOX-derived pro-inflammatory factors. On the other hand, HCR presented with a "shutdown" of COX-induced vasoconstriction and enhanced resolution of inflammation to maintain vascular tone and homeostasis. In conclusion, LCR display low-grade chronic inflammation via increased COX activity. These results provide mechanistic clues as to why lower intrinsic aerobic capacity correlates with a predisposition to risk of vascular disease. Conversely, being born with higher intrinsic aerobic capacity is a significant factor for improved vascular physiology in female rats.
Identifiants
pubmed: 33872803
pii: S1537-1891(21)00034-3
doi: 10.1016/j.vph.2021.106862
pmc: PMC8448916
mid: NIHMS1694757
pii:
doi:
Substances chimiques
Arachidonic Acid
27YG812J1I
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
106862Subventions
Organisme : NIH HHS
ID : P40 OD021331
Pays : United States
Organisme : NHLBI NIH HHS
ID : K99 HL151889
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL149762
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL151889
Pays : United States
Organisme : NIGMS NIH HHS
ID : R00 GM118885
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
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