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      La adventicia: estado actual del conocimiento Translated title: The Adventitia: Current State of Knowledge

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          Abstract

          La adventicia se ha definido como la capa de tejido conectivo más externa de un vaso y no formaría una unidad con la estructura vascular. El término "adventicia" proviene del latín adventicius, que significa "venido de afuera, extraño". Estos conceptos tal vez constituyan la causa de la subestimación del papel fisiológico de esta túnica. Al presente es bien conocido que la adventicia contiene vasa vasorum y nervi vasorum con funciones nutricionales y de control, respectivamente. A ello se suma la presencia de factores bioquímicos que serían responsables de cambios en la conducta elástica y viscosa de la pared arterial a través de una regulación de la función muscular lisa. En este trabajo se realiza una síntesis del papel estructural y fisiológico de la adventicia; se analizan además datos clínicos y experimentales que se comparan con resultados originales publicados por el autor.

          Translated abstract

          The adventitia has been defined as the outermost connective tissue covering of a vessel, and does not form an integral part of the vascular structure. The term "adventitia" comes from the Latin word adventicius, meaning "coming from abroad, foreign". These concepts may explain why the physiological role of this tunic has been underestimated. It is well known that the adventitia has vasa vasorum and nervi vasorum with nutritional and control functions, respectively. In addition, biochemical factors may probably account for changes seen in elastic and viscous behaviour of the arterial wall due to changes in smooth muscle function. This study reports a summary of the structural and physiological role of the adventitia: clinical and experimental data are also analyzed and compared with the original outcomes published by the author.

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          Most cited references83

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          Plaque neovascularization is increased in ruptured atherosclerotic lesions of human aorta: implications for plaque vulnerability.

          Growth of atherosclerotic plaques is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica media into the base of the plaque and by lumen-derived microvessels through the fibrous cap. Microvessels are associated with plaque hemorrhage and may play a role in plaque rupture. Accordingly, we tested this hypothesis by investigating whether microvessels in the tunica media, the base of the plaque, and the fibrous cap are increased in ruptured atherosclerotic plaques in human aorta. Microvessels, defined as CD34-positive tubuloluminal capillaries recognized in cross-sectional and longitudinal profiles, were quantified in 269 advanced human plaques by bicolor immunohistochemistry. Macrophages/T lymphocytes and smooth muscle cells were defined as CD68/CD3-positive and alpha-actin-positive cells. Total microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, microvessel density was increased in lesions with severe macrophage infiltration at the fibrous cap (P=0.0001) and at the shoulders of the plaque (P=0.0001). In addition, microvessel density was also increased in lesions with intraplaque hemorrhage (P=0.04) and in thin-cap fibroatheromas (P=0.038). Logistic regression analysis identified plaque base microvessel density (P=0.003) as an independent correlate to plaque rupture. Thus, neovascularization as manifested by the localized appearance of microvessels is increased in ruptured plaques in the human aorta. Furthermore, microvessel density is increased in lesions with inflammation, with intraplaque hemorrhage, and in thin-cap fibroatheromas. Microvessels at the base of the plaque are independently correlated with plaque rupture, suggesting a contributory role for neovascularization in the process of plaque rupture.
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            Periadventitial fat releases a vascular relaxing factor.

            Virtually all blood vessels are surrounded by adventitial fat. Adipocytes produce a host of vasoactive substances that may influence vascular contraction. We tested whether or not perivascular adipose tissue modulates contraction of aortic ring preparations. We studied aortic rings surrounded by periadventitial adipose tissue from adult Sprague-Dawley rats. At a maximum concentration of 300 nM angiotensin II, 6.5 microM serotonin, and 5 microM phenylephrine, the contractile response of intact rings was 95%, 80%, and 30% lower than that of vessels without periadventitial fat. The anticontractile effect of periadventitial fat was reduced by inhibition of ATP-dependent K+ channels with glibenclamide (3 microM) and by the tyrosine kinase inhibitor genistein (10 microM). Blocking NOS, cyclo-oxygenase, cytochrome P450, or adenosine receptors did not restore the vascular response in intact vessels. The anticontractile effect of perivascular fat was present in Zucker fa/fa rats, suggesting that leptin receptors were not responsible. Transferring the bath solution from intact vessels, isolated periadventitial tissue, and cultured rat adipocytes to precontracted vessels lacking periadventitial fat resulted in a rapid relaxation. We suggest that perivascular adventitial adipose tissue releases a transferable adventitium-derived relaxing factor that acts by tyrosine kinase-dependent activation of K+ channels in vascular smooth muscle cells.
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              Visceral periadventitial adipose tissue regulates arterial tone of mesenteric arteries.

              Periadventitial adipose tissue produces vasoactive substances that influence vascular contraction. Earlier studies addressed this issue in aorta, a vessel that does not contribute to peripheral vascular resistance. We tested the hypothesis that periadventitial adipose tissue modulates contraction of smaller arteries more relevant to blood pressure regulation. We studied mesenteric artery rings surrounded by periadventitial adipose tissue from adult male Sprague-Dawley rats. The contractile response to serotonin, phenylephrine, and endothelin I was markedly reduced in intact vessels compared with vessels without periadventitial fat. The contractile response to U46619 or depolarizing high K+-containing solutions (60 mmol/L) was similar in vessels with and without periadventitial fat. The K+ channel opener cromakalim induced relaxation of vessels precontracted by serotonin but not by U46619 or high K+-containing solutions (60 mmol/L), suggesting that K+ channels are involved. The intracellular membrane potential of smooth muscle cells was more hyperpolarized in intact vessels than in vessels without periadventitial fat. Both the anticontractile effect and membrane hyperpolarization of periadventitial fat were abolished by inhibition of delayed-rectifier K+ (K(v)) channels with 4-aminopyridine (2 mmol/L) or 3,4-diaminopyridine (1 mmol/L). Blocking other K+ channels with glibenclamide (3 micromol/L), apamin (1 micromol/L), iberiotoxin (100 nmol/L), tetraethylammonium ions (1 mmol/L), tetrapentylammonium ions (10 micromol/L), or Ba2+ (3 micromol/L) had no effect. Longitudinal removal of half the perivascular tissue reduced the anticontractile effect of fat by almost 50%, whereas removal of the endothelium had no effect. We suggest that visceral periadventitial adipose tissue controls mesenteric arterial tone by inducing vasorelaxation via K(v) channel activation in vascular smooth muscle cells.
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                Author and article information

                Contributors
                Role: ND
                Journal
                rac
                Revista argentina de cardiología
                Rev. argent. cardiol.
                Sociedad Argentina de Cardiología (Ciudad Autónoma de Buenos Aires, , Argentina )
                1850-3748
                February 2008
                : 76
                : 1
                : 58-63
                Affiliations
                [01] Buenos Aires orgnameFavaloro University Argentina
                [02] orgnameCONICET orgdiv1Research Career
                Article
                S1850-37482008000100012
                f6d89e4c-08cd-4d26-9f0f-f0c258784c56

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 50, Pages: 6
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                SciELO Argentina


                Elasticity,Viscosity,Vasa vasorum,Arteries,Arterias,Elasticidad,Viscosidad

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