The thoracic perivascular adipose tissue spontaneously induces vasoconstriction through activation of
Leonardo Gomes-Pereira1, José Eduardo da Silva-Santos1
1Department of Pharmacology, Laboratory of Cardiovascular and Smooth Muscle Biology, Universidade Federal de Santa Catarina, Florianópolis, Santa Catarina, Brazil.
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 PSSt(+)PVAT, which was transferred (t) to the organ baths and analysed for noradrenaline content.
Key Results:
Transfer (t) of the PSSt(+)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 PSSt(+)PVAT. Guanethidine also promoted vasoconstriction in aortic rings fully attached to PVAT. The contractile responses evoked by PVAT were abolished by prazosin, an α1-adrenoceptor antagonist. Immunoassay detection revealed that the contractile effects mediated by the PSSt(+)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.
More Related Videos
Related Concept Videos
Adrenergic Receptors: β Subtype
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors...
Adrenergic Receptors (Adrenoceptors): Classification
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors,...
Adrenergic Receptors: ɑ Subtype
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase...
Sympathetic Signaling
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Thoracic Aorta
Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally,...


