AI Article Synopsis

  • The study explored how perivascular adipose tissue (PVAT) interacts with endogenous and exogenous hydrogen sulfide (HS) in the thoracic aorta of normotensive and hypertensive rats.
  • In spontaneously hypertensive rats (SHRs), PVAT exhibited an anticontractile effect but also negatively impacted endothelial-dependent vasorelaxation, while HS had mixed effects on vasorelaxation depending on the rat strain.
  • Overall, the findings suggest PVAT may aggravate endothelial function in SHRs, but HS from the vascular wall promotes relaxation, indicating a potential compensatory mechanism for regulating vascular tone.

Article Abstract

The objective of this study was to investigate the vasoregulatory role of perivascular adipose tissue (PVAT) and its mutual interaction with endogenous and exogenous HS in the thoracic aorta (TA) of adult normotensive Wistar rats and spontaneously hypertensive rats (SHRs). In SHRs, hypertension was associated with cardiac hypertrophy and increased contractility. Regardless of the strain, PVAT revealed an anticontractile effect; however, PVAT worsened endothelial-dependent vasorelaxation. Since HS produced by both the vascular wall and PVAT had a pro-contractile effect in SHRs, HS decreased the sensitivity of adrenergic receptors to noradrenaline in Wistar rats. While HS had no contribution to endothelium-dependent relaxation in Wistar rats, in SHRs, HS produced by the vascular wall had a pro-relaxant effect. We observed a larger vasorelaxation induced by exogenous HS donor in SHRs than in Wistar rats. Additionally, in the presence of PVAT, this effect was potentiated. We demonstrated that PVAT of the TA aggravated endothelial function in SHRs. However, HS produced by the TA vascular wall had a pro-relaxation effect, and PVAT revealed anti-contractile activity mediated by the release of an unknown factor and potentiated the vasorelaxation induced by exogenous HS. All these actions could represent a form of compensatory mechanism to balance impaired vascular tone regulation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8946625PMC
http://dx.doi.org/10.3390/biom12030457DOI Listing

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