Book of Abstracts - New Frontiers 2022

Abstracts of poster presentations

THE ROLE OF INTERACTION BETWEEN PERIVASCULAR ADIPOSE TISSUE AND HYDROGEN SULFIDE IN VASOACTIVE RESPONSES OF THORACIC AORTA IN HYPERTRIGLYCERIDEMIC RATS

S. Čačányiová 1 , S. Golas 1 , M. Cebová 1 , M. Majzúnová 1,2 , H. Malínská 3 , A. Berényiová 1

1 Institute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, Bratislava, Slovakia; 2 Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia; 3 Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic Dysfunction of arterial smooth muscle cells and perivascular adipose tissue (PVAT) as main sources of vasoactive substances such as hydrogen sulfide (H 2 S) interferes with the ethiopathogenesis of different pathological stages, such as hypertension or metabolic syndrome. However, the mutual relationship between activity of PVAT and H 2 S effects has not been fully investigated to date. In spontaneously hypertensive rats, we confirmed that H 2 S signal pathway in interaction with PVAT could serve as reserved mechanism of NO deficiency. The aim of this study was to evaluate the mutual relationship among PVAT, endogenous and exogenous H 2 S in vasoactive responses of isolated thoracic aorta in hypertriglyceridemic (HTG) rats used as model of metabolic syndrome. 18-20-weeks-old male normotensive Wistar and HTG rats were used. Systolic blood pressure (sBP) was measured by plethysmography. Serum levels of glucose and lipids were measured using commercially available kits. Endothelium-dependent vasorelaxation induced by acetylcholine (Ach) and noradrenaline (NA)-induced contraction of TA with preserved PVAT+ or denuded PVAT- were recorded as changes in isometric tension. The pre-treatment with propargylglycine (PPG, 10 mM) was used to inhibit H 2 S producing enzyme. Na 2 S·9H 2 O was used to evaluate the vasoactive effect of exogenous H 2 S. Statistical significance was determined using an ANOVA followed by a Bonferroni post hoc test on raw data. Compared to Wistar rats, 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 H 2 S producing enzyme, and an altered oxidative state. In HTG, endogenous H 2 S 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 H 2 S. Although we observed a higher vasorelaxation induced by exogenous H 2 S donor in HTG rats than in Wistar rats, intact PVAT subtilized this effect. Our results confirmed that in hypertriglyceridemic rats, endogenous H 2 S could manifest dual effect depending on the type of triggered signaling pathway. H 2 S produced in the vessel wall contributed to endothelial dysfunction; however, the anti-contractile action of PVAT was associated with H 2 S activity as probable part of compensatory mechanisms. In experimental model of metabolic syndrome, the presence of PVAT determined the character (pathological vs compensatory) of effect of endogenously produced H 2 S.

Keywords: hydrogen sulfide, perivascular adipose tissue, thoracic aorta, vasoactivity, hypertriglyceridemic rats

Funding: VEGA 2/0147/22, APVV-20-0421

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