Axon potential, Muscle, Endocrine Flashcards
Flux
J = PdeltaC, units of mol/(cm^2*hr)
Permeability coeff
P = KD/membrane thickness (X), units of cm/hr
Partition coeff
K = solubility in oil : solubility in water
P-type transporter
primary AT, E-P intermediate, Ex: Na/K ATPase, Ca ATPase, H/K ATPase
F-type transporter
primary AT, H pump run in reverse to make ATP
Cardiac glycosidases
Inhibits Na/K ATPase, ex: digoxin, digitoxin
ABC transporters
primary AT, MDR and CFTR receptors
Reflection coeff (sigma)
= 0 (permeable solute), = 1 (impermeable solute)
Nernst equation
[-60/z]*log[Xi]/[Xo]
GHK equation
[-60/z]*log(Pk[Ki]+PNa[Nai]+PCl[Clo)]/(Pk[Ko]+PNa[Nao]+PCl[Cli])
Titin
connects Z-lines to thick filaments, runs from M-line to Z-line, provides horizontal stability
Nebulin
Sets length of thin filaments to 1.05um, important for anchoring capping proteins
Tropomodulin
actin capping protein, protects from depolymerization at one end
CapZ
actin capping protein, protects from depolymerization at one end, anchors thin filament to Z-line proteins ie alpha-actinin
Alpha-actinin
Anchors thin filaments to Z-line
Thick filament
3 peptide chains, 1 heavy, 2 light, S1 (ATPase and actin binding site), S2 (neck), and tail region
Thin filament
double stranded helix of actin monomers, with tropomyosin (extends over 7 actin filaments) and troponin (TnT, TnC, TnI)
Cross bridge cycle
1) AM (rigor) myosin head bound to actin in 45deg angle
2) A + M-ATP, ATP binds and myosin head is released from actin in 45 deg angle
3) A + M-ADP-Pi, ATP is hydrolyzed, moves to 90deg angle, RESTING STATE
4) AM-ADP-Pi, myosin binds to actin IF Ca++ is present and has bound to TnC and moved tropomyosin out of the way, revealing actin binding site
5) AM, power stroke occurs when ADP-Pi leaves
Isotonic
Same force, myosin detaches and binds to DIFFERENT actin molecule, shortening occurs
Isometric
Same length, myosin detaches and binds to SAME actin molecule, force is generated
Striated muscle is always turned ?
ON! only inhibited by troponin/tropomyosis, turned on when Ca++ binds to TnC of troponin, this is disinhibition
T-tubules
Extracellular tubular system on invaginations of sarcolemma
Sarcoplasmic reticulum
Intracellular tubular system which stores Ca++, has longitudinal part with Ca++ ATPase and terminal cisternea which stores Ca-calsequestrin
Contraction in skeletal muscle
DHR act as voltage-sensor proteins and move foot processes our of the way so RYR can release Ca++ from SR, muscle relaxes through Ca++ ATPase in longitudinal SR which pumps Ca++ out of the cytosol into SR, no extracellular Ca++, contraction is all or none