AI Article Synopsis
- Healthy perivascular adipose tissue (PVAT) has an important role in regulating vascular tone by exerting an anticontractile effect on resistance arteries, which is influenced by β-adrenoceptor activation and the release of adiponectin.
- Studies showed that electrical stimulation of PVAT releases an anticontractile factor that can reduce contractility in nearby blood vessels, demonstrating that sympathetic nerve activity plays a significant role in this process.
- In mechanisms that involve β-adrenoceptors and adiponectin, the absence of adiponectin (in knockout mice) removes the anticontractile effect, highlighting the essential function of PVAT in vasodilation.
Article Abstract
Objective: Healthy perivascular adipose tissue (PVAT) exerts an anticontractile effect on resistance arteries which is vital in regulating arterial tone. Activation of β-adrenoceptors by sympathetic nerve-derived NA (noradrenaline) may be implicated in this effect and may stimulate the release of the vasodilator adiponectin from adipocytes. Understanding the mechanisms responsible is vital for determining how PVAT may modify vascular resistance in vivo.
Approach And Results: Electrical field stimulation profiles of healthy C57BL/6J mouse mesenteric resistance arteries were characterized using wire myography. During electrical field stimulation, PVAT elicits a reproducible anticontractile effect, which is endothelium independent. To demonstrate the release of an anticontractile factor, the solution surrounding stimulated exogenous PVAT was transferred to a PVAT-denuded vessel. Post-transfer contractility was significantly reduced confirming that stimulated PVAT releases a transferable anticontractile factor. Sympathetic denervation of PVAT using tetrodotoxin or 6-hydroxydopamine completely abolished the anticontractile effect. β-adrenoceptor antagonist SR59203A reduced the anticontractile effect, although the PVAT remained overall anticontractile. When the antagonist was used in combination with an OCT3 (organic cation transporter 3) inhibitor, corticosterone, the anticontractile effect was completely abolished. Application of an adiponectin receptor-1 blocking peptide significantly reduced the anticontractile effect in +PVAT arteries. When used in combination with the β-adrenoceptor antagonist, there was no further reduction. In adiponectin knockout mice, the anticontractile effect is absent.
Conclusions: The roles of PVAT are 2-fold. First, sympathetic stimulation in PVAT triggers the release of adiponectin via β-adrenoceptor activation. Second, PVAT acts as a reservoir for NA, preventing it from reaching the vessel and causing contraction.
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| http://dx.doi.org/10.1161/ATVBAHA.118.310777 | DOI Listing |
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