Abstract
Our understanding of the regulation of vascular function, specifically that of vasomotion, has evolved dramatically over the past few decades. The classic conception of a vascular system solely regulated by circulating hormones and sympathetic innervation gave way to a vision of a local regulation. Initially by the so-called, autacoids like prostacyclin, which represented the first endothelium-derived paracrine regulator of smooth muscle. This was the prelude of the EDRF-nitric oxide age that has occupied vascular scientists for nearly 30 years. Endothelial cells revealed to have the ability to generate numerous mediators besides prostacyclin and nitric oxide (NO). The need to classify these substances led to the coining of the terms: endothelium-derived relaxing, hyperpolarizing and contracting factors, which included various prostaglandins, thromboxane A2, endothelin, as well numerous candidates for the hyperpolarizing factor. The opposite layer of the vascular wall, the adventitia, eventually and for a quite short period of time, enjoyed the attention of some vascular physiologists. Adventitial fibroblasts were recognized as paracrine cells to the smooth muscle because of their ability to produce some substances such as superoxide. Remarkably, this took place before our awareness of the functional potential of another adventitial cell, the adipocyte. Possibly, because the perivascular adipose tissue (PVAT) was systematically removed during the experiments as considered a non-vascular artifact tissue, it took quite long to be considered a major source of paracrine substances. These are now being integrated in the vast pool of mediators synthesized by adipocytes, known as adipokines. They include hormones involved in metabolic regulation, like leptin or adiponectin; classic vascular mediators like NO, angiotensin II or catecholamines; and inflammatory mediators or adipocytokines. The first substance studied was an anti-contractile factor named adipose-derived relaxing factor of uncertain chemical nature but possibly, some of the relaxing mediators mentioned above are behind this factor. This manuscript intends to review the vascular regulation from the point of view of the paracrine control exerted by the cells present in the vascular environment, namely, endothelial, adventitial, adipocyte and vascular stromal cells.
Highlights
Physiologists ascribed the regulation of the vascular tone to hormones released by specific endocrine glands or to the autonomous nervous system
It is known that resistin impairs endothelial function (Kougias et al, 2005), omentin elicits minor endothelium-dependent relaxations (Yamawaki et al, 2010) and vaspin improves endothelium-dependent relaxations elicited by acetylcholine (Kameshima et al, 2016)
In contrast with these three, chemerin has been demonstrated to be generated by perivascular adipose tissue (PVAT), with pro-contractile (Watts et al, 2013) as well as endothelium dysfunctioning (Neves et al, 2014) properties, acting possibly via NAD(P)H oxidase (Neves et al, 2015) and potentiating the effects of adrenergic nerve endings within PVAT (Darios et al, 2016)
Summary
Physiologists ascribed the regulation of the vascular tone to hormones released by specific endocrine glands or to the autonomous nervous system. Discovery of a vasodilatory prostaglandin synthesized and released by the vessel wall Chemical structure and coining of the term: prostacyclin The endothelium as the most abundant source of prostacyclin Activation of guanylate cyclase by NO and nitrocompounds Discovery of the role of endothelium as a source of vasodilating substances upon stimulation Earliest confirming reports Endothelium-dependent vasoconstriction First use of the acronym: EDRF First use of the term: nitrovasodilators Endothelium-dependent hyperpolarization of smooth muscle Existence of an endothelial cell-derived vasoconstrictor substance of polypeptidic nature Evidence of endothelial release of a diffusible vasoconstrictor substance Endothelium-dependent contractions are mediated by endothelial prostaglandins Incorporation of the acronym: EDCF Chemical nature of EDRF as NO Earliest confirming reports Identification of L-arginine as the precursor of NO Isolation of endothelin Incorporation of the term: EDHF Endothelial release of a diffusible hyperpolarizing substance Influence of perivascular adipose tissue on smooth muscle responsiveness Assignment of a paracrine role to adventitial cells Adventitium-derived relaxing factor coined as ADRF Demonstration that ADRF hyperpolarizes smooth muscle cells Incorporation of the acronym: PVAT Existence of a procontractile transferable substance from PVAT Tunica adiposa as the fourth layer of the vascular wall histologically acknowledged Incorporation of the term: perivascular adipocyte-derived constricting factor PVCF Incorporation of the term: adipocyte-derived hyperpolarizing factor ADHF
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