Cardio 2: Smooth Muscle Flashcards
SM
Main populations surround
“hollow organs”:
blood vessels, airways, GI tract, uterus and Fallopian tubes, ureters and bladder
SM
Also important in (2)
ocular function, piloerection
SM Contraction may cause (2)
propulsion or resistance
SM
Stimulus for contraction may be
intrinsic
SM
“Involuntary”: regulated by
efferent autonomic neurons, hormones,
and autocrine/paracrine signals
SM cell size
Smaller cells with single central nucleus
SM Specialized for (3) contractions (compared to skeletal muscle)
slow, steady, long
Specialized for slow, steady, long contractions (compared to skeletal muscle) (4)
- Contractions are slower to develop (1/10 to 1/300 speed)
- Contractions last significantly longer (30x longer)
- Maximum force generation greater (up to 2x greater/cm2)
- Primarily oxidative metabolism
SM cell shape
elongated &
tapered
SM striation
Smooth muscle is non-striated (
Smooth muscle lacks —
and only has rudimentary
T-tubules
SR
Types of Smooth Muscle (2)
multi unit single unit (unitary visceral)
Multi-unit (6)
No Gap Junctions Each cell responds independently Muscle behaves as multiple units Control exerted mainly by nerve signals Cells function independently No tone
Single-Unit (Unitary, Visceral) (6)
Cells connected by gap junctions Functional Syncytium Control by variety of stimuli Pacemaker cells Cells organizes into sheets or bundles May have tone
Smooth myocytes contain (2)
actin & myosin
Actin (3)
- Higher levels and longer than in skeletal/cardiac myocytes
- Alpha actinin attaches actin to dense bodies (Intracellular and
Membrane bound) - Arranged diagonally to long axis of cell
Myosin (2)
- Fewer myosin fibers than skeletal/cardiac myocytes
- Myosin Filaments interspersed with actin
Smooth myocytes lack —
troponin
Calcium binds to —
Calmodulin
Two actin-binding proteins: (2)
a. Calponin inhibits myosin ATPase
b. Caldesmon inhibits myosin/actin bond
Contraction results in — — of cell
rounding up
May contract efficiently over a wide
range of
resting lengths
Requirements for contraction: (3)
- Calcium (*Extracellular/Some Intracellular)
- ATP for contraction (myosin head has an ATPase)
- Myosin Light Chain Phosphorylation
- Calcium (*Extracellular/Some Intracellular) (2)
Binds to calmodulin for contraction
Removes calponin & caldesmon from actin
- Myosin Light Chain Phosphorylation (3)
Required for myosin head to interact with Actin
Myosin light chain kinase – adds phosphate and begins contraction
Myosin light chain phosphatase – removes phosphate and stops contraction
Smooth muscle contraction can be stimulated by (3)
- Stretch
- Ligands (neurotransmitters/hormones/paracrines/autocrines)
- Intrinsic activity (pacemaker cells)
Action potentials are not necessarily required for — in contractile force
increases
Many smooth muscle cells (ex: vascular) are — smooth muscle cells.
tonic
They are normally contracted (have “tone”), but can alter their force of contraction.
Cross-Bridge Activation: (5)
Cross-bridge cycling in smooth muscle is controlled by a Ca2+ regulated enzyme that phosphorylates myosin.
Only the phosphorylated form of smooth muscle myosin can bind to actin and undergo cross-bridge cycling.
This is done by myosin light chain kinase (MLCK).
To relax a contracted smooth muscle, myosin must be dephosphorylated because dephosphorylated myosin is unable to bind to actin.
Dephosphorylation is mediated by the enzyme myosin light-chain phosphatase (MLCP)
Two sources of Ca2+ : (2)
1. The sarcoplasmic reticulum. 2. Extracellular Ca2+ entering the cell through plasma-membrane Ca2+ channels.
To relax, the Ca2+ has to be removed: (2)
To SR via Ca++ ATPase
To ECF via Ca++ ATPase and Na+/Ca++ Exchanger
Cross Bridge Cycling in Smooth Muscle (2)
A.Attachment of myosin to actin depends on the phosphorylation of the myosin by myosin light chain kinase (MLCK; activated by calcium- calmodulin) B. Phosphorylated cross-bridges continue to cycle (myosin ATPase is active) until myosin phosphatase dephosphorylates the myosin head. Probably never get complete relaxation unless remove calcium.
When myosin is
dephosphorylated, myosin and
actin may form
latch-bridges
Tension is maintained although
Ca++ levels in cytosol — and ATP
usage —
decreases
decreases
When myosin is phosphorylated, cross bridges repeatedly form & break if --- is present
ATP
Latch State —
sustained contraction at low cost.
Tonic contractions creating smooth muscle tone.
Several mechanisms influencing
smooth muscle cell activation
Input to smooth muscle can be either
excitatory or inhibitory.
inputs influencing smooth muscle contractile activity (5)
spontaneous electrical activity in the PM of the muscle cell
NT released by autonomic neurons
hormones
locally induced changes in the chemical composition (paracrine factors, acidity, oxygen, osmolarity, and ion concentrations) of the extracellular fluid surrounding the cell
stretch
Smooth Muscle Activation: Autonomic Motor Neurons
Do not form —
synapses
Smooth Muscle Activation: Autonomic Motor Neurons
Axons have —
Varicosities
Smooth Muscle Activation: Autonomic Motor Neurons
NT released into
interstitial
fluid
Smooth Muscle Activation: Autonomic Motor Neurons
Distribute to receptors on
smooth muscle cell surface
via
simple diffusion.
Smooth Muscle Activation: Autonomic Motor Neurons
Each smooth muscle cell
may be influenced by more
than one
varicosity
Smooth Muscle Activation: Autonomic Motor Neurons
(2) contraction
Stimulate or inhibit
Depending on Receptor
May or may not induce – change
(2) contraction
Vm
Activate or inhibit
Local factors, including (5), can also
alter smooth muscle tension.
paracrine signals, acidity, O2 and CO2 levels, osmolarity, and the ion composition of the extracellular fluid
Responses to local factors provide a means for
altering smooth muscle
contraction in response to changes in the muscle’s immediate internal
environment, independent of long-distance signals from nerves and
hormones.
Many of these local factors induce
smooth muscle relaxation (ex. Nitric
oxide (NO)).
Some smooth muscles can also respond by contracting when they are
stretched
Stretching opens
mechanosensitive ion channels, leading to
membrane depolarization. The resulting contraction opposes the forces
acting to stretch the muscle.
Pacemaker Potentials (4)
Pacemaker smooth muscle cells Resting membrane not stable, slow depolarization to threshold Mechanism unknown Pacemaker Cells found in GI Tract (contract rhythmically without input)
