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Flashcards in Local Blood Flow Regulation Deck (31)
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dense bodies

structures that actin filaments attach to in smooth muscle cells in the interior of the cell

correlates to the Z-line


dense bands

structures where actin filaments attach to the inner surface of the cell


latched state

the state of contraction in smooth muscle that can be maintained by low energy consumption

probably involves very slow cycling or even non-recycling cross-bridges


regulation of smooth muscle contractile activity

changes in intracellular free calcium levels

changes in calcium sensitivity of the contractile machinery


calcium release from the SR in smooth muscle

voltage operated calcium channels

receptor operated calcium channels

chemical activation (IP3) of calcium release calcium binds with calmodulin to activate myosin light chian kinase, promoting contraction


mechanisms for smooth muscle contraction

protein kinase C linked receptors

coupled via a G protein to phospholipase C

IP3 causes calcium release from SR

DAG activates PKC


mechanisms for smooth muscle relaxation

calcium is pumped back into the SR

nitric oxide generated cGMP inhibits myosin kinase and promotes relaxation


factors regulating vascular smooth  muscle contraction

activity of symathetic nerves

agents produced and/or secreted by the endothelium

factors in circulation such as hormones, catecholamines, blood gases


renin-angiotensin system

angiotensin -> angiotensin I (through renin) -> angiotensin II (through ACE)

angiotensin II receptors are of the AT1 subtype

leads to vasoconstriction and aldosterone release



process by which a change in the perfusion pressure is countered by a change in resistance in the vascular bed that kepes flow relatively constant


theories for mechanisms of autoregulation



tissue pressure


myogenic mechanism of autoregulation

the vascular smooth muscle contracts in response to stretch and relaxes with a reduction in the stress


metabolic mechanisms of autoregulation

blood flow is linked to the metabolic activity of the tissue

a change in the oxygen supply will produce a change in the amount of a "metabolite" that is vasoactive


tissue pressure mechanism of autoregulation

a change in perfusion will produce a change in the interstitial pressure, which will change the external force on the blood vessels in the tissue

most operable in tightly encapsulated tissue (limited compliance)



imbalance between oxygen supply and demand that leads to a relative increase in blood flow

functional - due to increased metabolism

reactive - due to metabolic debt


endothelial factors

nitric oxide


endothelin 1

endothelial dependent hyperpolarizing factor  (EDHF)



an arachidonic acid metabolite with actions similar to NO

released from endothelial cells in response to many stimuli including hypoxia, shear stress, acetylcholine, and platelet products such as serotonin

causes relaxation of vascular smooth muscle through cAMP mechanisms


endothelial dependent hyperpolarizing factor (EDHF)

also acts like nitric oxide

hyperpolarizes adjacent vascular smooth muscle cells and causes relaxation


endothelin 1

potent vasoconstrictor

produced by endothelial cells in response to stimuli

under normal circumstance, vasodilator influences predominate


nitric oxide synthesis


interaction of endothelium with platelets

in the absence of vascular injury, the vasodilators regulate platelet interaction and vessel dilation

in the case of injury, vasodilators are downregulated, and this promotes vessel contraction as well as allows platelet aggregation


promoters of vascular growth

vascular endothelial growth factor (VEGF) - tyrosine kianse receptor

fibroblast growth factors (FGFs) - embryonic, fetal, and postnatal development

angiopoietin-1 (ANGPT1) - endothelial cells, required for embryonic vascular development


inhibitors of vascular growth

EC matrix of tumros and breakdown product of collagen XVII to make endostatin

angiostatin from plasminogen - enhanced apoptosis of endothelial cells

angiopoietin-2 (ANGPT2) - antagonist of ANGPT1



potent vasoconstrictor and cardiac stimulant

beta1 - chronotropic for heart

beta2 - dilates muscle vessels

alpha receptors lead to vasoconstriction in the veins and vasodilation in the arterioles due to the beta2 effect



similar effect as epinephrine on beta1

relatively little beta2 effect

increases peripheral resistance and both diastolic and systolic BP

alpha receptors lead to vasoconstriction on both the venous and arterial sides

leads to vagal reflex, so HR is not increased



potent agonist of both beta1 and 2

minimal to no effects on alpha receptors


parasympathetic innervation of the heart

Ach binds muscarinic receptors in nodes and muscle, leads to slowing of heart and AV conduction

only small changes in contractility


basal arterial tone

theoeretical reference point

amount of vascular contractions during resting conditions

assumed that no neural factors are present


resting sympathetic tone

amount of vascular contraction found under resting conditions as a result of tonic sympathetic nerve activity

resistance is higher than the basal arterial tone due to presence of a tonically released vasoconstrictor, NE


overall effect of circulating epinephrine

moderate increase in arterial blood pressure (due to increased cardiac output