Cell Physiology Flashcards
ex. cell conc. of Na
ECF [Na+]=?
145 mEq/L
ICF PH
7.2
EXF PH= 7.4
ICF slightly more acidic
The expression of this identifying protein is down-regulated in virally infected cells.
- Important cell surface protein that plays a functional role in immunity.
MHCI- functions in identifying self vs. non-self
ECF and ICF conc.’s of Mg2+ and Ca<strong>2+</strong>
Greater ECF concentrations but still very little.
[Ca2+]ICF = 10-4
[Mg2+]ECF = 1-2 mEq/L
[Ca2+]<span>ECF</span> = 0.5
ECF conc. Cl-
110 mEq/L
Just like Na+, there is higher ECF conc.
Osmolarity
Osmolarity= concentration of particles (Osm/L)
g =number of particles in solution (Osm/mol)
[e.g., gNaCl = 2; ~ucose = 1] C = concentration (mol/L)
Two solutions that have the same calculated osmolarity are isosmotic. If two solutions have different calculated osmolarities, the solution with the higher osmolarity is hyperos- motic and the solution with the lower osmolarity is hyposmotic.
Osmolarity eq.
Compare osmolarity of 1M CaC12 and 1M KCl
isotonic, hypertonic, hypotonic solutions
Osmolarity=g.C.RT
Theosmoticpressureincreaseswhenthesoluteconcentrationincreases.Asolutionof1M CaC12 has a higher osmotic pressure than does a solution of 1 M KCl because, for a given volume, the number of osmotically active particles is higher.
The higher the osmotic pressure of a solution, the greater the water flow into it.
Two solutions having the same effective osmotic pressure are isotonic because no water flows across a semipermeable membrane separating them. If two solutions separated by a semipermeable membrane have different effective osmotic pressures, the solution with the higher effective osmotic pressure is hypertonic and the solution with the lower effective osmotic pressure is hypotonic. Water flows from the hypotonic to the hyper- tonic solution.
Reflection coefficient (σ)
is a number between zero and one that describes the ease with which a solute permeates a membrane.
a. If the reflection coefficient is one, the solute is impermeable. Therefore, it is retained in the original solution, it creates an osmotic pressure, and it causes water flow. Serum albumin (a large solute) has a reflection coefficient of nearly one.
b. If the reflection coefficient is zero, the solute is completely permeable. Therefore, it will not exert any osmotic effect, and it will not cause water flow. Urea (a small solute) usually has a reflection coefficient of close to zero and it is, therefore, an ineffective osmol e.
The pathophysiology of this protein (transporter) manifest in typeII diabetes
Insulin receptor (receptor protein)
ICF conc. of K+
140 mEq/L
The luminal enzyme of PCT of neophrons that interconverts carbon dioxide and water into proton and carbonate
luminal carbonate anhydrase- Generally requires Zn (considered metalloenzyme)
Pathophysiology of this enzyme causes proximal renal tubular acidosis
Luminal carbonic anhydrase located in proximal convoluted tubules (PCT) of nephrons.
The pathophysiology of this career protein causes diabetes mellitus
GLUT4- Glucose Sodium symporter
Composition of cytosol (relative to ECF)
ICF vs ECF composition
Differs markedly from ECF in terms of electrolytes and PH. Consists of intracellular fluid, which contains many soluble proteins, ions, metabolites, and cytoskeletal elements.
Nicotinic receptors on muscle cells are an example of:
- A class of protein
Transmembrane protein and function as Na+_gated ion channel
ECF PH=?
7.4
maximal effective osmotic pressure
Na+-gated channels
The activation gate of the Na+ channel in nerve is opened by depolarization.
The inactivation gate of the Na+ channel in nerve is closed by depolarization.
When both the activation and inactivation gates on Na+ channels are open, the channels are open and permeable to Na+ (e.g., during the upstroke of the nerve action potential).
If either the activation or inactivation gate on the Na+ channel is closed, the channel is closed and impermeable to Na+.
For example, at the resting potential, the activation gates are closed and thus the Na+ channels are closed.
If the intracellular [Na+] is 15 mM and the extracellular [Na+] is 150 mM, what is the equilibrium potential for Na”’?
ENa• = -60mV/z log (Ci)/(Co)
=-60mVIog 0.1
=+60mV
Resting membrane potential
- is approximately -70 mV, cell negative.
- is the result ofthe high resting conductance to K+, which drives the membrane potential toward the K+ equilibrium potential.
- At rest, although the inactivation gates on Na+ channels are open (having been opened by repolarization from the preceding action potential),theactivationgateson Na+ channels are closed and thus the Na+ channels are closed and Na+ conductance is low.
Upstroke of action potential
(1) Inward current depolarizes the membrane potential to threshold.
(2) Depolarization causes rapid opening of the activation gates of the Na+ channels. Now, both activation and inactivation gates are open and the Na+ conductance of the membrane promptly increases.
(3) The Na+ conductance becomes higher thanthe K+ conductance, and the membrane potential is driven toward (but does not quite reach) the Na+ equilibrium potential of+65 mV. Thus, the rapid depolarization during the upstroke is caused by an inward Na+current
(4) Theovershootisthebriefportionatthepeakoftheactionpotentialwhenthemem- brane potential is positive.
(5) Tetrodotoxin mxt and lidocaine block these voltage-sensitive Na+ channels and abolish action potentials.
Repolarization of action potential
(1) Depolarization also closes the inactivation gates ofthe Na+channels (but more slowly than it opens the activation gates). Closure of the inactivation gates results in clo- sure of the Na+ channels, and the Na+ conductance returns toward zero.
(2) Depolarization slowly opens K+ channels and increases K+conductance to even higher levels than at rest. Tetrathylammonium (TEA) blocks these votlate channels.
(3) The combined effect of closing the Na+ channels and greater opening of the K+ channels make the k conductance higher than the Na+ conductance and the membrane potential is repolarized. Thus, polarizaiton is caused by an outward K+ current
Synthesis and storage of ACh in the presynaptic terminal
Choline acetyltransferase catalyzes the formation of ACh from acetyl coenzyme A (CoA) and choline in the presynaptic terminal.
ACh is stored in synaptic vesicles with ATP and proteoglycan for later release.
Diffusion of ACh to the postsynaptic membrane (muscle end plate) and binding of ACh to
nicotinic receptors
The nicotinic ACh receptor is also a Na+ and r+ ion channel.
Binding of ACh to a subunits of the receptor causes a conformational change that opens the central core of the channel and increases its conductance to Na+ and K+. These are examples of ligand-gated channels.
EPP
End plate potential in the postsynaptic membrane
- Because the channels opened by ACh conduct both Na+ and K+ ions, the postsynaptic membrane potential is depolarized to a value halfway between the Na+ and K+ equilib- rium potentials (approximately 0 mV).
- The contents of one synaptic vesicle {one quantum) produce a miniature and plata potential (MEPP), the smallest possible EPP.
- MEPPs summate to produce a full-fledged EPP. Tha EPP is not an action potential, but simply a depolarization ofthe specialized muscle end plate.
EPSPs
Excitatorypostsynapticpotentials
- are inputs that depolarize the postsynaptic cell, bringing it closer to threshold and closer to firing an action potential.
- are caused by opening of channels that are permeable to Na+ and 1(+, similar to the ACh channels. The membrane potential depolarizes to a value halfway between the equilibrium potentials for Na+ and K+ (approximately 0 mV).
Excitatory neurotransmitters & Inhibitory neurotransmitters
Excitatory neurotransmitters include ACh, norepinephrine, epinephrine, dopa- mine, glutamate, and serotonin.
Inhibitory neurotransmitters are y-aminobutyric acid (GABA) and glycine.
Inhibitory postsynaptic potentials
are inputs that hyperpolarize the post synaptic cell, moving it away from threshold and farther from firing an action potential
are caused by opening Cl- channels. The membrane potential is hyperpolarized toward the cl- equilibrium potential (-90 mV).
