Why the study?
Although perivascular adipose tissue contains contractile substances, its vascular tone actions are mostly linked to anticontractile release; whether procontractile products exert direct effects remained unclear.
Perivascular adipose tissue from healthy rats can exert direct contractile effects on the thoracic aorta through the spontaneous release of noradrenaline and activation of α1-adrenoceptors.
Background and Purpose Although perivascular adipose tissue (PVAT) contains substances with contractile properties, its actions on the vascular tone are associated with the release of anticontractile substances. We hypothesize that procontractile PVAT products also exert direct effects on vascular tone. Experimental Approach Thoracic aortas from Wistar rats, with (E+) and without (E−) functional endothelium, were mounted in organ baths. Thoracic PVAT sections were incubated in physiological salt solution (PSS, 37°C or 70°C), yielding the PSS t (+)PVAT, which was transferred ( t ) to the organ baths and analysed for noradrenaline content. Key Results Transfer ( t ) of the PSS t (+)PVAT solution induced a sustained vasoconstriction, three times greater in E− than in E+ aortic rings. The contractile action of the thoracic PVAT did not differ between male and female rats and was also induced by abdominal and mesenteric PVAT. Exposure to heat (70°C) increased PVAT‐induced vasoconstriction by ~25 and 300% in E− and E+ rings, respectively. Incubation of PVAT with guanethidine increased the procontractile effects of PSS t (+)PVAT. Guanethidine also promoted vasoconstriction in aortic rings fully attached to PVAT. The contractile responses evoked by PVAT were abolished by prazosin, an α 1 ‐adrenoceptor antagonist. Immunoassay detection revealed that the contractile effects mediated by the PSS t (+)PVAT correlate with spontaneous or experimentally induced noradrenaline release by PVAT. Conclusions Using functional and transfer bioassay approaches, we showed that the PVAT from healthy rats can exert direct contractile effects in the thoracic aorta. Pharmacological approaches and quantitative determination indicate that the release of noradrenaline accounts for this action.
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Gomes‐Pereira et al. (2025) studied this question.
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