Smooth Muscle Flashcards
6 primary groups of smooth muscle in the body
vascular, GI, urinary, respiratory, reproductive, ocular
smooth muscle can be categorized in 3 ways
location, contraction pattern, single vs multi unit
tonic
continuously contracted (but can be variable)
phasic
periodic contraction and relaxtion
single unit smooth muscle cells
connected by gap junctions and the cell contracts as a single unit - most smooth muscle bc coordinated contraction (small intestines)
multi-unit smooth muscle cells
not electrically linked, and each cell must be stimulated independently - the eye
variscosities
although distinct motor end plates don’t exist, smooth muscle regulation by autonomic nerves - smooth muscles use less energy - sustains contraction for longer periods of time ex: bladder vs plank - work together
smooth muscle organization
intermediate filaments and protein dense bodies form the cytoskeleton. actin attaches to the dense bodies each myosin molecule is surrounded by actin filaments. smooth muscle- dense bundles maintain sturcture - 10 actin to 15 myosin
actin more dense in skeletal muscle 2:4
RMP in cardiac
-90 mV
smooth muscle RMP
-80 to -40 mV due to leakiness of Na+/Ca+
slow wave potentials
cyclic depolarization and repolarization allows for cyclic contraction of cells resulting in waves of peristalsis that sweep through the GI tract
leak currents
mediated by Na + and Ca+ entering through the voltage independent non selective cation channel. upstroke of an action potential is from ca2+ entering the cell via VGCC
electrochemical coupling
contraction caused by an electrical signals
pharmacomechanical coupling
chemical signals change muscle tension through signal transduction pathways with little or no change membrane potential - NT, paracrine, stretch and various hormones may result in contractions of smooth muscle without first eliciting an action potential - most still require influx of Ca2+
sources of intracellular ca2+
- Ca2+ increases due to entry through VGCC or from SR
there is some Ca induced Ca release and RyR but most from SR-released Ca from IP3 binding to IP3 receptors on SR
biochemistry of SM contraction
- intracellular Ca inc when Ca enters cell and released from SR
- Ca binds to calmodulin (CaM)
- Ca-CaM activates myosin like chain kinase (MLCK)
- MLCK phosphorylates and activates light chains in myosin heads and increases myosin ATPase activity
- active myosin cross bridges slide along actin and create muscle tension
(NT can elicit a contraction outside the cell)
GPCR-phospholipase C transduction
- signal molecule activates receptor and G protein
- G protein activates phospholipase C (PLC) - amplifier enzyme
- PLC converts membrane phospholipids into diacylglycerol (DAG) which remains in the membrane and IP3 which diffuses into the cytoplasm
- DAG activates protein kinase C (PKC) which phosphorylates proteins
- IP3 causes release of Ca2+ from organelles creating a Ca2+ signal
effect of phosphorylation : MLCK
kinases groups of enzymes that add a phosphate to different proteins - myosin is phosphorylated by MLCK - increases myosin’s ability to interact with actin - when MLCK is phosphorylated it is inactivated!
biochemistry of SM relaxation
- free Ca in cytosol decreases when Ca is pumped out of the cell or back into the SR
- Ca unbinds from CaM, MLCK activity dec
- mysoin phosphatase removes phosphate from MLCK which dec myosin ATPase activity
- less myosin ATPase activity results in dec muscle tension
most relax doesn’t happen this way
inc cAMP in cardiac vs SM
elevation of cAMP in cardiac increase HR contraction
SM cAMP in relaxes - activates myosin phosphatase which causes phosphate to be removed from myosin light chains which dec myosin ATPase activity
cAMP dependent relaxation of smooth muscle
activation of PKG - phosphorylation of MLCK - decreased phosphorylation of myosin
