Ch. 20 - Smooth Muscle

Front 1

smooth muscles

Back 1

- cells are surrounded by a net reticular fibers
- various diameters
- arranged in sheets
- lack highly structured neuromuscular junctions
- numerous bulbous swellings called varicosities
- less developed SR
- T tubules are absent

Front 2

single-unit smooth muscle

Back 2

- in walls of hollow visceral organs
- except heart
- have pacemaker cells allowing cells to contract rhythmically
- cell connected by gap junction
- cells have synchronous contraction

Front 3

multi-unit smooth muscle

Back 3

- airways of lungs
- large arrector pili muscles
- internal eye muscles that adjust pupil size
- muscle fibers are structurally independent
- cells work independently of each other
- no gap junctions

Front 4

ratio of thick and thin filaments

Back 4

- much lower in smooth than skeletal muscle
- thick filaments of smooth muscle have actin heads along entire length
- not connected at Z line

Front 5

smooth muscle cytoskeleton

Back 5

- bundles of thick and thin filaments criss-cross
- anchored to cell membrane at attachment junctions or plaques and within cell at dense bodies
- intermediate filaments form mesh with PM
- twist during contraction
- thicker and shortened

Front 6

lacks troponin

Back 6

- dense body acts like Z line of striated muscle
- contains alpha actin that anchors actin
- contains vimentin and desmin IF
- contains vinculin that binds integral membrane proteins

Front 7

caveolae

Back 7

- numerous invaginations of plasma membrance
- vesicular
- help bring in calcium needed for contraction
- equivalent to T-tubule system in striated muscle
- work with SR to sequester calcium when isn't needed for contraction
- major source of Ca
- regulate Ca = open and close

Front 8

regulatory scheme 1

Back 8

- Ca2 may enter from the extracellular fluid through channels in plasmalemma or caveolae
- open when muscle is electrically stimulated or plasmalemma is depolarized by excess k

Front 9

calcium is released from SR

Back 9

- receptor activation causes Ca to be released from SR
- activated receptor interacts with a G protein
- G protein activates phospholipase C (PLC)
- PLC hydrolyzes phosphatidyl inositol biphosphate
- one product of hydrolysis is inositol 1,4,5-triphosphate (IP3)
- IP3 binds to its receptor on surface of SR
- opens Ca channels and Ca from SR enters the myoplasm

Front 10

regulatory schemes

Back 10

- controlled by myosin binding site on actin and actin binding site on myosin

Front 11

smooth muscle contraction

Back 11

- Ca combines with calmodulin (CaM)
- Ca-CaM complex activates MLCK
- MCLK phosphorylates the myosin head
- hydrolyze ATP to ADP an Pi both of which bind to head
- myosin forms a cross bridge with actin

Front 12

regulatory scheme 2

Back 12

- Ca/calmodulin (CaCM) binds a protein = caldesmon
- caldesmon normally bound to thin filaments but removed when CaCM bind
- tropomyosin changes it location in helical grooves of F-actin
- exposes myosin binding site on actin
- Ca depleted the CaCM dissociates, caldesmon released and reassociates with thin filament

Front 13

caldesmon

Back 13

- prevents myosin binding to actin
- blocks myosin binding site on actin
- replaces troponin as calcium dependent regulator of tropomyosin's location
- Ca present = released
- phosporylation by several kinases (MAO kinase) and dephosphorylation by phosphatases regulate caldesmon actin-binding activity

Front 14

low Ca concentrations

Back 14

- caldesmon binds to troponin and actin
- reduce binding of myosin to actin
- keep muscle in relaxed state

Front 15

higher Ca concentrations

Back 15

- Ca-calmodulin complex binds to caldesmon releasing it from actin
- myosin can interact with actin
- muscle can contract

Front 16

long contractions

Back 16

- muscle has cross bridges that remain in a latch state even after Ca is removed
- ATP replaces ADP slowly
- MLCK and MLC phosphates may be involved

Front 17

regulation of contraction

Back 17

- neural regulation by autonomic nerves
- hormones like gastrin
- stretch provokes contraction
- local factors: low oxygen, histamine, excess CO2