The aim of this study was to evaluate the mutual relationship among perivascular adipose tissue (PVAT) and endogenous and exogenous H₂S in vasoactive responses of isolated arteries from adult normotensive (Wistar) rats and hypertriglyceridemic (HTG) rats, which are a nonobese model of metabolic syndrome. In HTG rats, mild hypertension was associated with glucose intolerance, dyslipidemia, increased amount of retroperitoneal fat, increased arterial contractility, and endothelial dysfunction associated with arterial wall injury, which was accompanied by decreased nitric oxide (NO)-synthase activity, increased expression of H₂S producing enzyme, and an altered oxidative state. In HTG, endogenous H₂S participated in the inhibition of endothelium-dependent vasorelaxation regardless of PVAT presence; on the other hand, aortas with preserved PVAT revealed a stronger anticontractile effect mediated at least partially by H₂S. Although we observed a higher vasorelaxation induced by exogenous H₂S donor in HTG rats than in Wistar rats, intact PVAT subtilized this effect. We demonstrate that, in HTG rats, endogenous H₂S could manifest a dual effect depending on the type of triggered signaling pathway. H₂S within the arterial wall contributes to endothelial dysfunction. On the other hand, PVAT of HTG is endowed with compensatory vasoactive mechanisms, which include stronger anti-contractile action of H₂S. Nevertheless, the possible negative impact of PVAT during hypertriglyceridemia on the activity of exogenous H₂S donors needs to be taken into consideration.

中文翻译：

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血管周围脂肪组织和硫化物信号通路在非肥胖代谢综合征模型中的血管活性作用


本研究的目的是评估成年正常血压 (Wistar) 大鼠和高甘油三酯 (HTG) 大鼠（非肥胖模型）离体动脉血管活性反应中血管周围脂肪组织 (PVAT) 与内源性和外源性 H ₂ S 之间的相互关系。代谢综合征。在HTG大鼠中，轻度高血压与葡萄糖耐受不良、血脂异常、腹膜后脂肪量增加、动脉收缩力增加以及与动脉壁损伤相关的内皮功能障碍有关，并伴有一氧化氮（NO）合酶活性降低、一氧化氮合酶表达增加H ₂ S 产生酶，并且氧化状态改变。在HTG中，无论PVAT是否存在，内源性H ₂ S都参与抑制内皮依赖性血管舒张作用。另一方面，保留PVAT的主动脉显示出更强的抗收缩作用，至少部分由H ₂ S介导。虽然我们观察到HTG大鼠中外源H ₂ S供体诱导的血管舒张作用比Wistar大鼠更高，但完整的PVAT削弱了这种作用。我们证明，在 HTG 大鼠中，内源性 H ₂ S 可以根据触发信号通路的类型表现出双重作用。动脉壁内的H ₂ S导致内皮功能障碍。另一方面，HTG的PVAT具有代偿性血管活性机制，包括更强的H ₂ S抗收缩作用。然而，高甘油三酯血症期间PVAT对外源性H ₂ S供体活性可能产生的负面影响需要考虑考虑在内。