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22 Cards in this Set

  • Front
  • Back
Smooth muscle properties
short, single nucleus, non striated, NO myofibrils, NO sarcomeres, have actin and myosin, electrically coupled by gap jxns, involuntary, ANS control and local control

layers in tubes and organs
smooth muscle capillaries contract the tunica...
media; capillaries and some smaller venues do not have SMCs
SMC contraction
AP--> MB depol--> VG Ca2+ channels--> increase Ca2+ in ICF--> Ca2+ binds calmodulin--> activates MLCK--> P-Myosin + actin--> contract
(MLC phosphatase--> myosin deP--> relaxation)
Myosin light chain phosphorylation
allows myosin-actin binding and contraction in SMCs
myosin heavy chain = contractile
myosin light chain = regulatory
Sources of Ca2+ in SMC
L type VG, ligand gated ca2+ channels, SR has RyR Ca2+ gated, SERCA pumps (puts ca2_ away), NCX (na+/ca2+ exchanger), ca2+ atpase pumps (pumps ca2+ out)
explain how contraction and tension development can occur when intracellular ca2+ levels decrease
b/c of phosphorylation
SMC unique cause it can stay contracted even after put ca2+ away because of the phosphorylation
can change contractile state of SMC at any given ca2+ level
SMC contracts b/c of other ca2+ independent signaling pathways can affect MLCK and MLCP
mechanism that endothelial derived hyperpolarizing factors (H2O2) causes VSMC relaxation
H2O2--> K+ hyperpol--> relax
amlodipine
DHPYR ca2+ antagonist--I influx of ca2+ (binds more SMC vs. cardiac cells)--> peripheral arterial vasodilator--> reduces peripheral vascular resistance and decrease BP
Nitroglycerine
dilate veins--> returns less blood to the heart--> heart works less
targets mostly the veins
NO--> guanylate cyclase--> increase cGMP in SMC--> dephospho rylation of MLC--> regulate contractile state in SMC--> vasodilation
nitroglycerine mech
nitroglycerine--> NO--> guanylate cyclase--> cGMP--> PKG--> MLCP--> myosin dephosphorylates--> relaxation
Tadalafil (--------> creates more cGMP)
NO from parasympathetic nerves and endothelial cells--> cGMP--> SMC relaxation--> increased blood flow into corpus cavernoum
tadalafil + sex stimulation--I PDE5--> enhances erectile fan by increasing cGMP
nitroglycerine mech
nitroglycerine--> NO--> guanylate cyclase--> cGMP--> PKG--> MLCP--> myosin dephosphorylates--> relaxation
PDE5
changes cGMP--> GMP
need sexual activity b/c need NO to be active
gotta turn on NO to have any effect on GC to make cGMP, which then PDE5 can work on to create GMP
Tadalafil (--------> creates more cGMP)
NO from parasympathetic nerves and endothelial cells--> cGMP--> SMC relaxation--> increased blood flow into corpus cavernoum
tadalafil + sex stimulation--I PDE5--> enhances erectile fan by increasing cGMP
can't give NO and tadalafil together
b/c target same pathways so will extremely vasodilator
PDE5
changes cGMP--> GMP
need sexual activity b/c need NO to be active
gotta turn on NO to have any effect on GC to make cGMP, which then PDE5 can work on to create GMP
epinephrine
SKM blood flow increases, skin blood flow decreases, airways in lungs increase in diameter
can't give NO and tadalafil together
b/c target same pathways so will extremely vasodilator
epinephrine
SKM blood flow increases, skin blood flow decreases, airways in lungs increase in diameter
3 ways to reduce blood pressure by targeting and II pathway
ACE--> angiotensin II--> AT1R--> rhoa and rhoK
1. inhibit AT1R
2. ACE inhibitors
3. rhoa and rhoK inhibit
Control of vascular tone local, metabolic, hormonal, and neural control
Hormonal--> EPI, ANGII
Neural control--> Ach, NO, NEPI
Local--> ENDO, NO, H2O2, hitamine
Metabolic--> CO2 build up, K, O2 decreases, adenosine, ATP