Concept map to compare and contrast the structure and ...

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Concept map to compare and contrast the structure and function of arteries and veins

Blood vessels are flexible tubes that carry blood, associated oxygen, nutrients, water, and hormones throughout the body. Learning ObjectivesDifferentiate among the structure of arteries, veins, and capillaries Key Points Blood vessels consist of arteries, arterioles, capillaries, venules, and veins. Vessel networks deliver blood to all tissues in a directed and regulated manner. Arteries and veins are composed of three tissue layers. The thick outermost layer of a vessel (tunica adventitia or tunica externa ) is made of connective tissue. The middle layer ( tunica media ) is thicker and contains more contractile tissue in arteries than in veins. It consists of circularly arranged elastic fibers, connective tissue, and smooth muscle cells. The inner layer ( tunica intima ) is the thinnest layer, comprised of a single layer of endothelium supported by a subendothelial layer. Capillaries consist of a single layer of endothelium and associated connective tissue. tunica intima: The innermost layer of a blood vessel. tunica externa: The outermost layer of a blood vessel. capillary: Any of the small blood vessels that connect arteries to veins. tunica media: The middle layer of a blood vessel. anastomosis: The junction between blood vessels. Blood vessels are key components of the systemic and pulmonary circulatory systems that distribute blood throughout the body. There are three major types of blood vessels: arteries that carry blood away from the heart, branching into smaller arterioles throughout the body and eventually forming the capillary network. The latter facilitates efficient chemical exchange between tissue and blood. Capillaries in turn merge into venules, then into larger veins responsible for returning the blood to the heart. The junctions between vessels are called anastomoses. Arteries and veins are comprised of three distinct layers while the much smaller capillaries are composed of a single layer. The inner layer (tunica intima) is the thinnest layer, formed from a single continuous layer of endothelial cells and supported by a subendothelial layer of connective tissue and supportive cells. In smaller arterioles or venules, this subendothelial layer consists of a single layer of cells, but can be much thicker in larger vessels such as the aorta. The tunica intima is surrounded by a thin membrane comprised of elastic fibers running parallel to the vessel. Capillaries consist only of the thin endothelial layer of cells with an associated thin layer of connective tissue. Surrounding the tunica intima is the tunica media, comprised of smooth muscle cells and elastic and connective tissues arranged circularly around the vessel. This layer is much thicker in arteries than in veins. Fiber composition also differs; veins contain fewer elastic fibers and function to control caliber of the arteries, a key step in maintaining blood pressure. The outermost layer is the tunica externa or tunica adventitia, composed entirely of connective fibers and surrounded by an external elastic lamina which functions to anchor vessels with surrounding tissues. The tunica externa is often thicker in veins to prevent collapse of the blood vessel and provide protection from damage since veins may be superficially located. Structure of the Artery Wall: This diagram of the artery wall indicates the smooth muscle, external elastic membrane, endothelium, internal elastic membrane, tunica externa, tunica media, and tunica intima. A major structural difference between arteries and veins is the presence of valves. In arteries, the blood is pumped under pressure from the heart, so backflow cannot occur. However, passing through the capillary network results in a decrease in blood pressure, meaning that backflow of blood is possible in veins. To counteract this, veins contain numerous one-direction valves that prevent backflow. AbstractEndothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the first of a 2-part review focused on phenotypic heterogeneity of blood vessel endothelium. This review provides an historical perspective of our understanding of endothelial heterogeneity, discusses the scope of phenotypic diversity across the vascular tree, and addresses proximate and evolutionary mechanisms of endothelial cell heterogeneity. The overall goal is to underscore the importance of phenotypic heterogeneity as a core property of the endothelium.The endothelium forms the inner cellular lining of blood vessels. Endothelial cells (ECs) are not inert but, rather, are highly metabolically active. The endothelium plays an important role in many physiological functions, including the control of vasomotor tone, blood cell trafficking, hemostatic balance, permeability, proliferation, survival, and innate and adaptive immunity. Endothelial cell phenotypes are differentially regulated in space and time, giving rise to the phenomenon of "EC heterogeneity." The endothelium has enormous yet largely untapped diagnostic and therapeutic potential. The goal of this review is to underscore the complexity of the endothelium and to emphasize the importance of approaching the endothelium as an integrated system.HistoryHippocrates and Galen viewed the vasculature as consisting of 2, unlinked systems of veins and arteries. Galen held that arteries contained air and vital spirits, whereas veins carried blood that was continuously formed in the liver. This erroneous theory of the circulation would hold sway for some 1500 years until William Harvey disproved Galen's hypothesis in 1628. Through a series of elegant physiological experiments in dogs, Harvey showed that the arteries and veins are in fact connected and that blood is contained within a closed circulation. Although he could not directly visualize the capillaries, Harvey surmised their existence. With the benefit of compound microscopy, Marcello Malpighi was the first to actually observe blood capillaries in 1661. The term endothelium was coined by the Swiss anatomist Wilhelm His in 1865, to differentiate the inner lining of body cavities from epithelium. The original definition included the cell lining of blood vessels, lymphatics, and mesothelial-lined cavities. The definition would later be narrowed to include only the inner cell layer of blood vessels and lymphatics.In the 1950s and 1960s, the use of electron microscopy (EM) provided a powerful new window into the endothelium. Early EM studies revealed the presence of characteristic organelles, including plasmalemmal vesicles (which are now called caveolae) and Weibel?Palade bodies.1 In addition, these investigations revealed--for the first time--the existence of structural heterogeneity. For example, in some vascular beds, ECs were tightly connected to one another and were surrounded by a continuous basement membrane (continuous endothelium). In a subset of these vascular beds, the ECs were permeated with holes or fenestrae (fenestrated endothelium). A third type of endothelium was characterized by the presence of fenestrae, frank gaps, and a poorly formed underlying basement membrane (discontinuous endothelium). The use of EM, together with tracers, led to revised theories of permselectivity and provided insights into the venular-specific regulation of permeability and leukocyte trafficking. These and other ultrastructural observations led Florey to conclude in 19662: Now it is recognized that there are many kinds of endothelial cells which differ from one another substantially in structure, and to some extent in function.The 1970s and 1980s ushered in a new era of cell biology. This was made possible by the first successful isolation and characterization of ECs in culture. In 1973 and 1974, Jaffe and colleagues3 and Gimbrone and colleagues4 independently reported the isolation of human ECs from the umbilical vein. The ability to culture ECs allowed investigators to manipulate--in a controlled manner --the extracellular environment and to study cell biology in far greater detail. Among the seminal findings of that time was the observation that incubation of cultured ECs with inflammatory mediators or bacterial products induced proadhesive, antigen-presenting and procoagulant activities, a phenomenon that was termed "EC activation."5?11Although the majority of research groups in the 1980s focused on cultured human umbilical vein ECs (and to a lesser extent, bovine aortic ECs), a small cadre of investigators used immunohistochemistry to characterize the endothelium in vivo. They reported that different vascular beds express different proteins.12?14 In other words, the intact endothelium displayed not only ultrastructural diversity, but also molecular heterogeneity. Implicit in these descriptive studies was a critical--if not largely overlooked--message, which was articulated by Auerbach and colleagues15: The concept that vascular endothelial cells are not all alike is not a new one to either morphologists of physiologists. Yet laboratory experiments almost always use endothelial cells from large vessels such as the human umbilical vein or the bovine dorsal aorta, since these are easy to obtain and can be readily isolated and grown in culture. The tacit assumption has been that the basic properties of all endothelial cells are similar enough to warrant the use of the cells as in vitro correlates of endothelial cell activities in vivo.Recognizing the importance of heterogeneity, Auerbach championed the use of cell cultures from multiple organ beds to study the biology of the endothelium. Such an approach would make most sense if vascular bed?specific phenotypes maintained their identity in vitro. As is discussed in a following section (Mechanisms of Endothelial Cell Heterogeneity), this assumption is only partially correct.Defining the EndotheliumHow do we define the endothelium? From an anatomical standpoint, the endothelium represents the inner cellular lining of the blood and lymphatic vessels. However, there are examples of vascular mimicry in which other cell types, eg, trophoblasts, form the inner lining of blood vessels. Many of the characteristic ultrastructural features of the endothelium, such as Weibel?Palade bodies or fenestrae, are not present in every EC. Other structures, such as caveolae, are not specific to the endothelium. Developmentally, endothelium arises from mesoderm via the differentiation of hemangioblasts and/or angioblasts (reviewed elsewhere16,17). However, other cell lineages may transdifferentiate into ECs, and ECs into other lineages.18,19 There are few, if any, protein/mRNA markers that are both specifically and uniformly expressed in the endothelium (reviewed elsewhere20). Of the leading candidates, platelet/endothelial cell adhesion molecule (PECAM)-1 (also known as CD31) is also expressed in monocytes; thrombomodulin in keratinocytes, trophoblasts, and leukocytes; and vascular endothelial (VE)-cadherin in trophoblasts and fetal stem cells. From a functional standpoint, the endothelium displays a remarkable "division of labor" (Table) (reviewed elsewhere21,22). Endothelial cells are typically "quiescent," in the sense that they are not actively proliferating (the average lifespan of an EC is more than 1 year). However, the endothelium of the corpus luteum and uterus undergo cyclical episodes of intense physiological proliferation.23 Finally, when endothelial-specific promoters are targeted to the mouse genome, they invariably fail to direct expression throughout the endothelium. Rather, they promote expression in specific subsets of ECs (reviewed elsewhere24). In summary, each of the above definitions falls short of fully capturing the endothelium. The "elusiveness" of the endothelium undoubtedly reflects its marked heterogeneity in structure and function. Table 1. Examples of Functional Heterogeneity of Endothelium in Normal Adult VasculatureFunctionPrimary SiteMechanismCommentsMHC indicates, major histocompatibility complex.PermeabilityBasalCapillariesIntercellular clefts, vesicle-mediated transcytosis, transendothelial channelsConstantly occurs across the endothelium, albeit at different rates between different vascular bedsInduciblePostcapillary venulesIntercellular clefts, vesicle mediated transcytosis, transendothelial channelsMay be physiological (localized, transient) or pathological (systemic, sustained, and/or excessive)Leukocyte transmigrationPostcapillary venules in skin, mesentery, muscle; capillaries in lung and liver; HEV in lymph nodesSite-specific repertoire of EC selectins, chemokines, and integrin ligandsMechanisms differ according to site, leukocyte subsetHemostasisPanvascularSite-specific repertoire of procoagulants and anticoagulantsSystemic imbalance in soluble factors will influence hemostatic balance in ways that differ between vascular beds, leading to focal thrombosisVasomotor toneArteriolesRelease of site-specific vasodilator and vasoconstrictor moleculesHumidificationBronchial microcirculationHigh surface area and close approximation to airwaysThermoregulationBronchial and skin microcirculationHigh surface area and close approximation to airways (bronchial microcirculation) and external environment (skin microcirculation)Vasoconstriction of cutaneous vessels conserves body heat; vasodilation and secondary elevation of blood flow to the skin promotes convective heat transfer from the core to the periphery of the bodySieve functionLiver sinusoidsFenestraeImportant for chylomicron clearanceScavengingLiver sinusoidsReceptor-mediated endocytosisImportant for clearance of gastrointestinal-derived bacterial products and particlesImmune toleranceLiver sinusoidsMHC class I and II molecules, costimulator moleculesTolerance to oral antigensProliferation/angiogenesisReproductive system (eg, ovary, uterus)Cyclical changes in expression of growth factorsStructural HeterogeneityThe shape of cells varies across the vascular tree. Although ECs are typically flat, they are plump or cuboidal in high endothelial venules (reviewed elsewhere25,26). Endothelial cell thickness varies from less than 0.1 m in capillaries and veins to 1 m in the aorta (reviewed elsewhere2). Endothelial cells (and their nuclei) are aligned in the direction of blood flow in straight segments of arteries but not at branch points.27,28 When canine arterial vessel segments were excised, rotated 90o, and reimplanted, the nuclear pattern of ECs realigned in the direction of blood flow within 10 days after surgery.29 Thus, flow-dependent alignment of ECs represents reversible endothelial structural remodeling in response to hemodynamic shear stress. In a study of rat blood vessels, aortic ECs were reported to be long and narrow (55?10 m) with their long axes oriented in the direction of blood flow; ECs of the pulmonary artery were broader and shorter (30?14 m), forming a rectangular shape; pulmonary vein ECs were large, and round in shape; and ECs of the inferior vena cava were long, narrow and rectangular.30 In the cremasteric muscle of mice, ECs of arterioles are longer than their counterparts in veins (length-to-width ratio 7.45 and 2.66, respectively) and have a higher surface area (1200 versus 600 m2, respectively).31 In a study of the tracheal microcirculation in rats, ECs were elongated and spindle shaped in arterioles; irregularly shaped in capillaries; large, elliptical, or irregularly shaped in postcapillary venules; and rounded in collecting venules.32 In scanning EM of the rat penis, EC nuclei in the deep artery were shown to leave elliptical depressions, whereas those in the helicine artery left deeper and more rounded depressions.33ECs possess clathrin-coated pits, clathrin-coated vesicles, multivesicular bodies and lysosomes, which represent the structural components of the endocytotic pathway (reviewed elsewhere34) (Figure 1). Endocytosis targets macromolecules to the lysosomal compartment for degradation. In some cases, endocytosed substances are recycled to the cell surface, or sorted to other subcellular compartments such as the Golgi and endoplasmic reticulum. Endocytosis takes place either by a nonspecific (fluid-phase) process or via receptor-dependent pathways. The latter process is mediated by so-called scavenger receptors, which are responsible for uptake of low-density lipoprotein (LDL), transferrin, albumin, ceruloplasmin, and advanced glycosylation end products. Liver sinusoidal ECs demonstrate particularly high rates of clathrin-mediated endocytosis. Figure 1. Endothelium and permeability. A, Capillaries mediate constitutive (albeit physiologically regulatable) transfer of solutes and fluids between blood and underlying tissue. In continuous nonfenestrated endothelium, water and small solutes (molecular radius,

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