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
Contraction in cardiac muscle
DHR act as voltage-gated calcium channels and respond to AP by letting a little Ca++ into the cell which triggers Ca++ release from the SR via the RYR - Calcium induced calcium release, need both Ca++ ATP for SR and Na/Ca exchanger (secondary AT) to remove Ca++ from the cytosol, contraction is graded, through prolonging plateau phase
PKA effects in cardiac muscle
1) phosphorylates TnI, increasing relaxation, and decreasing TnC affinity for Ca++
2) phosphorylates phospholamban on SR that increases CaATPase activity, increasing relaxation
Force production in skeletal muscle is controlled by what?
Neural control
How is skeletal muscle graded
Twitch, summation of force (repeated APs), tetanus (repetitive stimulation, rarely occurs physiologically)
Henneman Size Principle
recruitment of motor units within a muscle takes place with recruitment of larger and larger motor units
