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Plasma Membrane structure & Fxn
-limits mvmt of ions from IC to EC and vice versa
-permiable to hydrophobic subst
-ions and protein have low solubil.
Peripheral Proteins
attached to ONE surface of cell memb
ie antigens
Integral Proteins
Protrude through cell memb.
-provide channels through which H2O and other subst (ions) can pass
-fxn as txp protiens
Not always open
Integral Proteins
ion channels
carrier proteins-txp subs with low lipid sol
-txp subst AGAINST their conc grad.
play critical role in mvmt of ions
Gated ion channels
integral protien
-not always open
Factors controlling gated ion channels
chemical (receptor mediated)
electrical (voltage/RMP/AP)
Double gated ion channels
"M" gate on top (EC)
"H" gate on IC
Cell voltage
relatively (-) on IC side
sit on IC side of PL memb
sit on EC side of PL memb
cyclic nucleotide-gated ion channel
6 membrane spanning regions
binding site for cyclic nucleotides on IC
IC events hydrolize nucleotides-ie Ca++ channel, phosphorylation opens it at a given voltage
protein gets a phosphate-done by kinases
takes phos off of a protein
IC                            EC
K      140                          4
Na     10                           142
Cl      4                             103
Ca     0.0001                     2.4
-chg proteins
Ion gradients
-chg protiens are - and stay inside cell
-cell expends E to maintain ionic disbal
-plasma membrane helps to maintain
-cell without food leads to inability to make ATP, messes up ion gradient
Transmembrane voltage OR
Transmembrane potential
voltage diff across PM
due to IC and EC diff in ion conc.
how many of avail gates are open?
if conductance is increased, flow is increased

at rest most chan. are closed except some K+chann are open, allowing K= to diffuse out of cell (making IC more -)
# gates
Flow through gates
Factors affecting conductance
stretch, temperature, voltage
K+ greatest conductance
@ RMP (~-90mv)
K+chann open, diffuses from increased IC (140mm) to EC (4mm) concentration
-IC becomes more -
-rate of diffusion proportional to conc grad.
RMP influenced by
-EC ion concentration
-IC vs EC ion conc
-conc. of -chg molecules (which do not cross the PM)
-density of channels on the PM
-state of channels
-Na-K-ATPas pump activity/density
Nernst Equation (mv)
=61 log IC ion conc/EC ion conc
by electrical means alone, stops further diff. of an ion
Key Ion determining RMP
-K+ due to conductance of K+ channel
-also - chg proteins such as RNA, FA, proteins which cannot leave cell
Na/K+ ATP pump
pumps 3 Na molecules out of cell for every 2 K into cell

requires 1 molecule of ATP
Na/K ATP pump
against conc grad.
-translocation of Na creates an osmotic gradient that drives the abs of H2O
-creates electrical and chemical gradient
Export of Na with Na/K ATP pump
provides the driving force for several facilitated transporters, which import glucose, AA & other nutrients
Effect of no ATP
no ability to pump Na and K,
-RMP will increase to -70, cell supposed to be at rest, now at threshold=depol=tachyarrythmias
Effect of Elyte disturbances on RMP
change RMP
can cause depol esp in nerves and cardiac muscle
consequences = resp fail and card arrest
=gradient narrow, ch open with good conductance, high EC K prevents more K from moving across membrane.
RMP gets less -, closer to 0 = threshold and other channels open up
=depol= increased excitability= slightly high leads to tachycardia
very high leads to cardiac arrest "locked" in depol
increased gradient, increased flux, IC becomes more -, RMP more - (hyperpolarized), cell needs more stim to get to threshold = bradycardia
-normal 8.5-10.5mg/dl
-does not alter RMP directly
-Ca+ does regulate the number of Na chann open
-cells relatively impermiable to Ca
=more Na chan open
increased Na entry into cell
RMP becomes more +
increases HR slightly
fewer Na chan open
decreased Na entry into cell
RMP more -
decreases HR slightly
very little change in RMP for hyper/hyponatremia
Tx for intraop hyperkalemia
increases RMP (more -) hyperpolarizes
Differences btw cardiac and neuronal RMP
-mode of initiation
-ionic species
-speed of propogation
Cardiac conduction
SA node
R to L internodal tracts
then to AV node
then to bundle of HIS (AV bundle)
then RBB, LBB, purkinje fibers
ventricles (R then L)
Rates in SA node
AV node
ventricular cells
SA =100/min
AV =60/min
ventricle= 40/min
what is unique about the SA node?
spontaneous depol
Internodal tracts
within atria
~6x faster than cell-cell communication
anterior, posterior and middle
pot for reentry arrythmias here
RMP -60, closer to threshold
AV node
slows impulse down from AV node due to higher resistance to tansmission of APs- more slow Ca+ chan, fewer gap jxn, closer to threshold (-70)
allows atrial blood to be pushed into ventricles
Gap Jxns
direct electrical comm. btw cells, increases cond. velocity
allows cardiac myocytes to contract in tandem
AV bundle
or Bundle of HIS
only link btw atrial and vent contraction
gives rise to purkinje system
many gap jxns, very fast cond. velocity
Purkinje fibers
super highway of conduction
increased permiability of gap jxns
shape of AP in non-PM cells
have plateau phase (slow Ca channels)
How do cells in the SA node generate spontaneous APs?

RMP ~-60 PM of SAN leaky to Na
-influx of + ions makes IC more +
-moves RMP closer to 0
K channels less leaky, keeps RMP closer to -60
@-60 Na funny channels open (slow)
SA node AP
1. Na leak (funny)
2. 2 types Ca chan open @-50
T type=short fast
L type=slow (@ -40)
3. threshold=depol
4. repol voltage gated K+chann open, @0mv, stays oen until voltage falls to -60
T type Ca channels
transient, open @-50 close @ -25
also chem gated (PNS &SNS) SNS increases opening
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