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59 Cards in this Set
- Front
- Back
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epicardium structure
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two layers, each composed of thin mesothelium and connective tissue with thin layer of fluid between the two layers (parietal outside and visceral inside)
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endocardium structure
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endothelium and connective tissue, continuous w/ blood vessels and lines whole inner surface of heart
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connective tissue of myocardium
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endomysium surrounds each myocyte to provide it w/ supportive framework (coordinates force and prevents slippage); thicker perimysium surrounds groups of myocytes to prevent malalignment between bundles
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how is spread of damage limited from cell to cell?
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gap junctions are blocked by prolonged increase in intracellular calcium
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desmosome vs adherens junction
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desmosome attaches to intermediate filaments while adherens junctions attach to actin
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titin
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molecular spring, attaches from Z line to M line and allows for passive elasticity of cardiac muscle (diastolic compliance)
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what happens during passive stretching of cardiac muscle?
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as sarcomere is first stretched, titin extends - during this time, length changes while tension stays relatively constant (low); after titin is fully extended, the elastic PEVK region changes conformation, which produces an increase in passive tension w/ increased length
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myosin heavy chain types in myocardial cells
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alpha = fast = primarily in the atrium; beta = slow = primarily in the ventricle (bottom)
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microRNA-208
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ensures coordinated reciprocal regulation of alpha and beta myosin heavy chain abundance (if alpha high, beta low and vice-versus)
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EC coupling in cardiac muscle
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calcium induced calcium release: calcium enters via DHPR (L type Ca channels) and this calcium activates SR calcium channels, which release more calcium into cell
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removal of calcium from myocyte after contraction
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2/3 removed to SR via calcium pump (ATPase), 1/3 removed to extracellular space via NCX (3 Na in for 1 Ca out)
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conduction pathway
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SA node -> atria -> AV node -> Bundle of His -> right, left anterior, left posterior branches -> Purkinje fibers -> ventricles
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Purkinje cells vs myocytes
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Purkinje cels are larger and paler (fewer myofibrils, more glycogen)
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what differentiates atrial myocytes?
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endocrine function: secrete natriuretic peptides (ANP) that regulate body fluid homeostasis in response to high BP
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blood velocity throughout body
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fastest in biggest arteries, slowest in capillaries (more overall area therefore slower velocity)
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intima contains... (4)
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endothelial cells (squamous), basal lamina, connective tissue oriented longitudinally, internal elastic lamina (arteries and large veins -> small veins may have incomplete lamina)
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media contains... (3)
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smooth muscle cells (muscular arteries > elastic arteries), elastic fibers (elastic arteries > muscular arteries > veins), collagen; all connective tissue can be oriented circumferentially or in a spiral
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adventitia contains... (5)
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external elastic lamina (arteries only, less prominent and less complete than internal elastic lamina), smooth muscle (esp large veins), loose connective tissue oriented longitudinally, vasa vasorum, nerves
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purpose of elastin in large arteries
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allows them to expand during ventricular systole (store energy), and then snap back during diastole, propelling arterial blood downstream
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arteries vs veins layers differences
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similar intima, arteries have larger media w/ more smooth muscle and less collagen than veins, similar adventitia (veins have higher % adventitia); thus arteries have thicker walls relative to their lumens; veins never have external elastic lamina (large veins may have incomplete internal elastic lamina while venules may not have any); vein layer boundaries are more indistinct
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layers in arterioles
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intima has endothelium w/ basal lamina, very thin layer of connective tissue, and possibly internal elastic lamina (missing in some arterioles); media has a few layers of circular smooth muscle (1 or 2 in arterioles), collage; adventitia is relatively thick, with loose connective tissue and sometimes external elastic lamina (missing in smallest arterioles)
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control of arteriole smooth muscle
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ANS, adrenal medulla catecholamines, locally produced endothelial factors (endothelin, NO, prostacyclin), local chemical environment aka autoregulation (O2, CO2, pH, lactic acid, adenosine)
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autoregulation
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control of arteriole smooth muscle by local chemical environment (O2, CO2, pH, lactic acid, adenosine) rather than ANS
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pericyte functions (around capillaries)
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may have a contractile function to modulate capillary flow; serve as progenitors of vascular smooth muscle during angiogenesis
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capillary structure
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intima only (no media or adventitia) -> only one endothelial cell layer, with or without basement membrane
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purposes of microcirculation vessels (3)
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arterioles regulate blood flow via smooth muscle; capillaries control permeability and exchange of substances; venules control permeability and leukocyte emigration
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control of capillary blood flow (3)
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smooth muscle sphincter at the origin of each capillary allows some capillaries in a bed to be perfused while others aren't; thoroughfare capillary channels are always perfused; some tissues (clitoris, penis, skin, nose, lips) have arteriovenous shunts to bypass capillary bed altogether
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mechs of exchange between capillary luman and extravascular space (3)
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passive diffusion across membranes (gases); pinocytosis (either non-specific w/o receptors - like for water, soluble proteins; or specific w/ receptors - like for LDL, transferrin); passage between endothelial cells in discontinuous capillaries and in post-capillary venules during leukocyte emigration
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capillary types: features, found where (3)
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continuous - most common (brain, muscle, skin, lung), endothelial cells w/ tight junctions and complete basal lamina, transport occurs by diffusion or pinocytosis; fenestrated - continuous basal lamina but pores exist between endothelial cells, fenestrated capillaries w/ diaphragms are in intestine, gall bladder, endocrine glands, renal tubules (areas important for absorption), fenestrated capillaries w/o diaphragms are in glomeruli; discontinuous capillaries have incomplete endothelial cell lining AND incomplete basal lamina, largest discontinuous caps are found in liver and spleen (sinusoids)
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fenestrated capillaries w/o diaphragms found where?
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renal glomeruli
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fenestrated capillaries w diaphragms found where? (4)
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intestine, gall bladder, endocrine glands, renal tubules
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discontinuous capillaries found where? (2)
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liver and spleen
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continuous capillaries found where? (4)
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most common: brain, muscle, skin, lung
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special relationships of endothelial cells w/ epithelial cells found where?
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blood-brain, blood-testis, blood-thymus barriers
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portal circulation types and examples
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portal arterial circulation: afferent arteriole -> glomerular cap -> efferent arteriole -> loops of Henle cap bed (ACE); portal venous circulation: gut capillaries -> portal veins -> hepatic sinusoids -> hepatic vein and hypothalamic capillaries -> portal veins -> anterior pit caps
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capacitance vessels
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veins, because they are more easily distended and thus can store more blood volume
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valves in veins
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semilunar
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function of: elastic arteries, muscular arteries, arterioles, capillaries, venules, veins
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elastic arteries: conductance (propel blood during diastole and thus dampen change in BP), muscular arteries: regional distribution of blood flow, arterioles: resistance (BP and local blood flow), capillaries: exchange, venules: cell migration, veins: capacitance
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anti/prothrombotic properties of endothelial cells
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us. inhibit platelets and coagulation, but with injury can promote platelet adherence and activation by decr prostacycline and thrombomodulin and promote thrombosis by exposure of tissue factor and von Willebrand factor
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Weibel-Palade bodies
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von Willebrand factor is stored in the cytoplasm of endothelial cells in these bodies
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endothelial cells make what factor?
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factor VIII (as well as vWF)
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endothelial cell derived factors that modulate smooth muscle function (3)
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NO and prostacycline promote vasodilation and prevent platelet adhesion; endothelin promotes vasoconstriction
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tonic vs phasic smooth muscle
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tonic smooth muscle is in a constant state of tension due to latch states (found in vascular tissue) while phasic smooth muscle contracts rhythmically (found in GI tract)
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vascular smooth muscle lacks vs skeletal muscle (4)
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sarcomeres, Z lines, troponin, T tubules
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vascular smooth muscle features (4)
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constant tension w/ little energy expenditure; multiple triggers of contraction (not just APs); can modulate contractile and secretory fns; ability to proliferate and migrate
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intermediate filaments in vascular smooth muscle vs other smooth muscle types
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vascular has both desmin and vimentin while other types only have desmin
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dense bodies
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actin filaments are anchored into dense bodies that contain alpha-actinin (either in cytoplasm or attached to membrane), dense bodies attach to each other and plasma membrane via intermediate filaments (desmin and vimentin)
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smooth muscle vs skeletal muscle abilities and cause (3)
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smooth muscle can shorten more b/c multiple directions of orientation and multiple sites of anchorage; smooth muscle has greater degrees of contraction and can maintain max contractile force at varying cell lengths b/c smooth muscle has more actin than myosin (myosin can change the actin they bind to) and b/c smooth muscle myosin can bind w/ each head to an actin filament w/ opp polarity (sidepolar cross bridges)
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how is smooth muscle re-lengthened?
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intermediate filaments are compressed during cell contraction, and they can act as a spring to re-lengthen the cell when the cell relaxes
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latch state
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tension-holding state of smooth muscle, where very little energy is needed to maintain tension
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sidepolar cross bridges
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found in smooth muscle because 2 heads of myosin can bind diff actin w/ diff polarity -> allows for more degrees of contraction
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bipolar cross bridges
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found in skeletal muscle because 2 heads of myosin bind actin filaments w/ same polarity -> allows for fewer degrees of contraction than smooth muscle
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EC coupling in smooth muscle
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calcium + calmodulin activates myosin light chain kinase, which phosphorylates the regulatory light chain at the myosin head end; phosphorylation of the RLC allows unfolding and polymerization of the myosin tail (in vitro phenomenon - the tail is always phosphorlyzed in vivo) and activation of ATP-hydrolyzing and actin-binding sites in the myosin head
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triggers for vascular smooth muscle contraction (4)
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elevated intracellular calcium is required: 1. action potential; 2. ligand (NE, angiotensin II, endothelin, vasopressin, thromboxane A2) binding to GPCR activates PLC, causing incr IP3, which causes Ca release from SR; 3. ligand binding opens ligand-sensitive plasma membrane calcium channels; 4. stretch-sensitive calcium channels
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relaxation of vascular smooth muscle overview and mechs (3)
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relaxation is caused by dephosphorylation of myosin light chain by MLC phosphatase -> balance between MLC kinase and MLC phosphatase determines activation vs relaxation: 1. ATP-dep calcium pumps remove calcium from cell, which decr MLC kinase activity; 2. ligand (epinephrine, histamine, prostacyclin) binds to GPCR -> activ AC -> cAMP -> decr MLC kinase activity; 3. NO -> activate GC -> cGMP -> PKC -> activation of MLC phosphatase (PDE can break down cGMP, and PDE is inhibited by Viagra)
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vascular smooth muscle migration occurs when? (2)
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into intima in atheroscelerosis, and into perivascular space in angiogenesis
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lymphatic vessel histology
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lined by endothelial cells w/ incomplete basal lamina and no tight junctions
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lymphangions
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valves in lymphatic vessels divide them into segments called lymphangions
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lymph color
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normally clear (no RBC), but can be milky (chylous) after high-fat meal
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