ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016
Dahl SS rats demonstrate enhanced aortic perivascular adipose tissue-mediated buffering of vasoconstriction through activation of NOS in the endothelium.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Female Dahl, but Not SS13Research square · 2026Article
- Presence and Variability of the Microbiome in Perivascular Adipose Tissue: A Whole-Genome Sequencing Study in Dahl SS Rats.Life (Basel, Switzerland) · 2026Article
- Review
- Male and female high-fat diet-fed Dahl SS rats are largely protected from vascular dysfunctions: PVAT contributions reveal sex differences.American journal of physiology. Heart and circulatory physiology · 2021Article
- Liver circadian clock disruption alters perivascular adipose tissue gene expression and aortic function in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Administration of recombinant human placental growth factor decreases blood pressure in obese hypertensive pregnant rats.Journal of hypertension · 2020Article
- The Local Regulation of Vascular Function: From an Inside-Outside to an Outside-Inside Model.Frontiers in physiology · 2019Review
- Genome-wide map of proximity linkage to renin proximal promoter in rat.Physiological genomics · 2018Article
- New actions of an old friend: perivascular adipose tissue's adrenergic mechanisms.British journal of pharmacology · 2017Review
- Increased mitochondrial ROS generation mediates the loss of the anti-contractile effects of perivascular adipose tissue in high-fat diet obese mice.British journal of pharmacology · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Perivascular adipose tissue (PVAT) mediates buffering of vasoconstriction through activation of endothelium-derived factors. We hypothesized that the PVAT of Dahl salt-sensitive (Dahl SS) rats has reduced ability to buffer vasoconstriction. Vascular reactivity experiments were performed on aortic rings with PVAT intact (+PVAT) or removed (-PVAT), and endothelium intact (+ENDO) or removed (-ENDO) from Dahl SS rats and control SS.13(BN) rats (Dahl SS rats that have had chromosome 13 completely replaced with that of the Brown Norway rat, rendering this strain insensitive to high-salt or high-fat diet-induced hypertension). Endothelial dysfunction, assessed by ACh-mediated vasorelaxation, was confirmed in aortic rings of Dahl SS rats. The +PVAT+ENDO aortic rings had indistinguishable phenylephrine-induced vasoconstriction between genotypes. In both strains, removal of PVAT significantly enhanced vasoconstriction. Dahl SS rat -PVAT+ENDO aortic rings displayed exaggerated vasoconstriction to phenylephrine vs. SS.13(BN) rats, indicating that PVAT-mediated buffering of vasoconstriction was greater in Dahl SS rats. Removal of both the ENDO and PVAT restored vasoconstriction in both strains. The nitric oxide synthase (NOS) inhibitor, N(ω)-nitro-L-arginine methyl ester (L-NAME), produced a similar effect as that seen with -ENDO. These data indicate that the function of the PVAT to activate endothelium-derived NOS is enhanced in Dahl SS compared with SS.13(BN) rats and, most likely, occurs through a pathway that is distinct from ACh-mediated activation of NOS. PVAT weight and total PVAT leptin levels were greater in Dahl SS rats. Leptin induced a significantly decreased vasoconstriction in -PVAT+ENDO aortic rings from Dahl SS rats, but not SS.13(BN) rats. In contrast to our initial hypothesis, PVAT in Dahl SS rats buffers vasoconstriction by activating endothelial NOS via mechanisms that may include the involvement of leptin. Thus, the PVAT serves a vasoprotective role in Dahl SS rats on normal-salt diet.
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