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Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor.
Life Sci. 2020 Aug 01; 254:117819.LS

Abstract

AIMS

Vascular dysfunction plays a key role in sepsis but the role of perivascular adipose tissue (PVAT) in this condition is relatively unknown.

MAIN METHODS

Sepsis was induced by cecal ligation and puncture (CLP). The responses of the aorta and superior mesenteric artery to norepinephrine in the presence or absence of PVAT were evaluated. Fluorescent probes measured the production of nitric oxide (NO) and reactive oxygen species (ROS). NO synthases (NOS) and β3-adrenoceptor expression were detected by immunofluorescence and S-nitrosylation by the biotin switch assay.

KEY FINDINGS

Aorta and superior mesenteric arteries from septic animals with intact PVAT showed a worsened response to the vasoconstrictor compared to vessels without PVAT. PVAT from the aorta (APVAT) produced NO and ROS whereas PVAT from the superior mesenteric artery (MPVAT) produced only ROS. Septic APVAT exhibited a higher density of NOS-1 and NOS-3. S-nitrosylation was found in APVAT. Donor (PVAT obtained from normal or septic rats):Host (normal vessel without PVAT) experiments showed that L-NAME, ODQ and β3-adrenergic receptor antagonist blocked the septic APVAT anti-contractile effect. None of these compounds affected MPVAT; tempol, but not apocynin, blocked its anti-contractile effect.

SIGNIFICANCE

PVAT contributes to the anti-contractile effect in the aorta and mesenteric artery of septic rats through different pathways. β3-Adrenergic receptor and NO appear to be key mediators of this effect in APVAT, but not in MPVAT where ROS seem to be a relevant mediator. Therefore, PVAT is a relevant player of sepsis vascular dysfunction.

Authors+Show Affiliations

Department of Pharmacology, Universidade Federal de Santa Catarina, SC, Brazil.Department of Pharmacology, Universidade Federal de Santa Catarina, SC, Brazil.Department of Pharmacology, Universidade Federal de Santa Catarina, SC, Brazil. Electronic address: jamil.assreuy@ufsc.br.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32442451

Citation

Barp, Clarissa Germano, et al. "Perivascular Adipose Tissue Phenotype and Sepsis Vascular Dysfunction: Differential Contribution of NO, ROS and Beta 3-adrenergic Receptor." Life Sciences, vol. 254, 2020, p. 117819.
Barp CG, Benedet PO, Assreuy J. Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor. Life Sci. 2020;254:117819.
Barp, C. G., Benedet, P. O., & Assreuy, J. (2020). Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor. Life Sciences, 254, 117819. https://doi.org/10.1016/j.lfs.2020.117819
Barp CG, Benedet PO, Assreuy J. Perivascular Adipose Tissue Phenotype and Sepsis Vascular Dysfunction: Differential Contribution of NO, ROS and Beta 3-adrenergic Receptor. Life Sci. 2020 Aug 1;254:117819. PubMed PMID: 32442451.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor. AU - Barp,Clarissa Germano, AU - Benedet,Patricia Oliveira, AU - Assreuy,Jamil, Y1 - 2020/05/19/ PY - 2020/02/14/received PY - 2020/05/13/revised PY - 2020/05/17/accepted PY - 2020/5/23/pubmed PY - 2020/5/23/medline PY - 2020/5/23/entrez KW - Nitric oxide KW - Perivascular adipose tissue KW - Reactive oxygen species KW - Sepsis KW - Vascular dysfunction SP - 117819 EP - 117819 JF - Life sciences JO - Life Sci. VL - 254 N2 - AIMS: Vascular dysfunction plays a key role in sepsis but the role of perivascular adipose tissue (PVAT) in this condition is relatively unknown. MAIN METHODS: Sepsis was induced by cecal ligation and puncture (CLP). The responses of the aorta and superior mesenteric artery to norepinephrine in the presence or absence of PVAT were evaluated. Fluorescent probes measured the production of nitric oxide (NO) and reactive oxygen species (ROS). NO synthases (NOS) and β3-adrenoceptor expression were detected by immunofluorescence and S-nitrosylation by the biotin switch assay. KEY FINDINGS: Aorta and superior mesenteric arteries from septic animals with intact PVAT showed a worsened response to the vasoconstrictor compared to vessels without PVAT. PVAT from the aorta (APVAT) produced NO and ROS whereas PVAT from the superior mesenteric artery (MPVAT) produced only ROS. Septic APVAT exhibited a higher density of NOS-1 and NOS-3. S-nitrosylation was found in APVAT. Donor (PVAT obtained from normal or septic rats):Host (normal vessel without PVAT) experiments showed that L-NAME, ODQ and β3-adrenergic receptor antagonist blocked the septic APVAT anti-contractile effect. None of these compounds affected MPVAT; tempol, but not apocynin, blocked its anti-contractile effect. SIGNIFICANCE: PVAT contributes to the anti-contractile effect in the aorta and mesenteric artery of septic rats through different pathways. β3-Adrenergic receptor and NO appear to be key mediators of this effect in APVAT, but not in MPVAT where ROS seem to be a relevant mediator. Therefore, PVAT is a relevant player of sepsis vascular dysfunction. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/32442451/Perivascular_adipose_tissue_phenotype_and_sepsis_vascular_dysfunction:_Differential_contribution_of_NO,_ROS_and_beta_3-adrenergic_receptor L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(20)30568-3 DB - PRIME DP - Unbound Medicine ER -