cardiovascular phys exam 3 part 2

how does the body overcome orthostasis (2)

skeletal muscle pump and precapillary vasoconstriction

why do muscles swell during exercise (3)

increased interstitial osmolarity, vasodilation, capillary recruitment

increased volume of interstitial fluid in tissue or organ

edema

what is anasarca edema

edema all over

what is acites edema

edema in the abdomen

a type of swelling where pressing a finger into the swollen tissue leaves a temporary indentation that slowly fills back in

pitting edema

what is a common cause of non-pitting edema

lymphedema

what are the four main causes of edema

increased capillary hydrostatic pressure, reduced capillary oncotic pressure, lymphatic obstruction, increased capillary permeability

what are the two common causes of edema of increased capillary hydrostatic pressure

impaired venous return and congestive heart failure

what are the three main causes of edema of reduced plasma oncotic pressure

low protein in diet, kidney failure, liver failure

build up of fluid when lymphatics damaged or blocked

edema of lymphatic obstruction

what is the most common cause of lymphadema in the US

cancer treatment

how can cancer treatment lead to lymphadema

if lymph nodes are removed, there is nothing to drain the lymph

what is the most common cause of lymphadema worldwide

filariasis, a parasite that lives in the lymphatics

what leads to edema of increased capillary permeability

gap formation in venules

protein fluid that leaks out

exudate

protein free fluid that leaks out

transudate

what intitates gap formation in edema of increased capillary permeability

contraction of myosin and disruption of tight junctions

what protein is missing from vascular smooth muscle cells

troponin

what initiates contraction in vascular smooth muscle cells

electrical or chemical signals or both

what controls contraction in vascular smooth muscle cells

myosin phosphorylation

can vascular smooth muscle cells replicate

yes, in response to injury or stress

are there t tubules in vascular smooth muscle cells

no

how big is the SR in VSMC

small, so there is less calcium

where are VSMC found

tunica media

what is the role of VSMC

supply mechanical strength and contractile power

what are the 4 important structures of VSMC

contractile units, dense bodies, calcium store, gap junctions

what do the dense bodies in VSMC do

anchor actin

where are the gap junctions in VSMC

between VSMC and VSMC as well as VSMC and endothelial cells

what do the gap junctions between VSMC and endothelial cells do

hyperpolarize VSMC leading to relaxation

what are the two kinds of calcium-release channels in VSMC

IP3 and ryanodine receptor

how do ryanodine receptors function in VSMC

a small calcium spark opens the receptors, allowing flow of calcium

what is essential for VSMC contraction

depolarization, not an action potential

when does myosin participate in contraction in VSMC

only when it is phosphorylated

what is troponin replaced by in VSMC

caldesmon and calponin

what activates myosin in VSMC

calcium

what is the first step in VSMC contraction

intracellular calcium increases

what happens after intracellular calcium increases in VSMC

calcium binds calmodulin

what happens after calcium binds calmodulin in VSMC

calcium-calmodulin complex activates myosin light chain kinase (MLCK)

what happens after MLCK is activated in VSMC

MLCK phosphorylates myosin

what happens after MLCK phosphorylates myosin

cross bridges form

how are cross bridges broken in VSMC

ATP binds to the myosin head, which breaks the cross bridge, but does not allow it to relax

what relaxes the myosin head in VSMC

myosin ligh chain phosphatase (MLCP) dephosphorylates the myosin head

what is the speed of VSMC conctraction compared to cardiac muscle

much slower, about 1/10 the speed

how do the contractile filaments in VSMC compare to cardiac muscle

they are much longer

how is force of VSMC contraction regulated

mostly by external stimuli, such as norepinephrine, epi, ang II, endothelin, serotonin, and histamine

how does the duration of VSMC contraction compare to cardiac muscle

it is typically sustained, because arteries maintain a state of partial contraction throughout life

what is a “latched” state crossbridge

a state where actin and myosin form crossbridges that remain in a locked state, where crossbridged form but do not break

how do latch crossbridges help conserve energy

they stay formed and recycle infrequently or not at all

which way does potassium flow

out

what do potassium channels do

hyperpolarize the cell

which way does calcium flow

in

what do calcium channels do

lead to contraction

which way does chloride flow

out

when do K_IR channels open

at moderate increases in intracellular potassium

what happens when K_IR channels open

hyperpolarization of the cell

what happens after the cell hyperpolarizes as a result of K_IR channels opening

voltage-sensitive calcium channels close

what happens after voltage-sensitive calcium channels close

no calcium coming in, so no contraction

when are K_IR channels mostly used

exercise

what do K_ATP channels do

link vascular tone to tissue metabolic state

what is the state of K_ATP channels when there is high ATP

closed

what is the state of K_ATP channels when there is low ATP

open

when are K_ATP opened to lead to hyperpolarization

suring hypoxia