BIPN 105 Human Mammalian Physiology Lab Final Study Guide

Receptors
nnAChR
nMAChR
m2AChR
m3AChR
AIIR
1
OTR
1
2

NT
ACh
ACh
ACh
ACh
AII
E, NE
OT
E, NE
E

Path

Gi
Gq
Gq
Gq
Gq
Gs
Gs

Neuron
Vrest = -70 mV / VT = -50 mV
Refractory period = 1 ms
Cond vel. = 20-100 m/s
Fatigue = no fatigue; hard to
disrupt [ion gradient]

Cell types
Neuron
Skeletal muscle
Nodal
Smooth muscle
Smooth muscle
Smooth muscle
Smooth muscle
Contractile, Nodal
Smooth muscle

Control

Parasymp
Symp

Symp

Effect

Tissues

Contract
HR, AV conduction
Contract/Relax
Contract (most potent constr. hormone)
Contract
Contract
Cont. duration, Cont. strength
Relax (decrease contraction)

Contracts: uterus, bladder, GI tract, bronchioles; Vasodilation via NO release

vasoconstriction
uterus, blood vessels
uterus, breast tissue

Skeletal Muscle
Vrest = -90 mV / VT = -50 mV
Refractory period = 3-4 ms
Cond vel. = 1 m/s
Fatigue = ACh vesicle depletion
Z line line up w t-tubules, actin
attached
I band actin only
A band myosin/actin overlap
A motor neurons - fast A,,,
C motor neurons - slow

Glutaminergic (glutamate)
excites CNS; most common
excitatory NT
GABAnergic (gamma
aminobutyric acid)
inhibits CNS
Adrenergic (NE)
sym ANS (postganglionic to
tissues, e.g. heart); CNS
Cholinergic (ACh) Nicotinic (mixed cation ch.)
nMAChR - NMJ
nNACHR - ANS (pregang to
postgang); CNS
Muscarinic
(mAChR) parasym ANS
(postgang to tissue); CNS
*block with Atropine
(muscarinic R competitive
antagonist)

nMAChR *2ACh/ nMAChR

CONTRACT
Na influx (0.15 ms) (small PK,
Vrest=EK)
Depolarize EPP
Activates v-gated Na ch. MAP
AP in T-tubule activates
DHPR/LTCC, pulls on protein to
open RyR-1 (releases SR Ca)
Ca binds Troponin/tropomyosin,
uncovers myosin binding sites =
Myo-act interaction =
crossbridge/powerstroke =
ATP ADP via myosin ATPase
== muscle contracts, shortens, T
*2 myosin heads, 2 ATPases per
molecule
*myosin ATPase always active
RELAX
SERCA-1 pumps Ca back into

blood vessels, uterus, bronchioles, eye muscles

(Vascular) Smooth Muscle

Fatigue = no fatigue; slow myo-act interaction means
slow increase in T and low ATP use
Single nuclei, small cells
Size: 2-5um diameter; 50-100um length
Myofilaments - not striated, shorten 50-75% (more
dynamic than striated); not arranged in sarcomeres
= Less crowding, Longer actin/myosin = easier
interactions
Contraction Duration: sec to min
- Prolonged Ca influx (LTCC)
- Slow Ca removal
- Can fire multiple APs (can summate)
PARASYMP
m3AChR (Gq) - contracts uterus, bladder, GI tract,
bronchioles; vasodilates vascular endothelial cells via
NO release
HORMONES
OTR (OT) (Gq) uterus, breast tissue
AIIR (AII) (Gq) most potent vasoconstr. hormone
SYMP
1 (NE,E) (Gq) uterus, blood vessels
Activates PLC (PIP2 DAG; IP3 byproduct)
IP3 activates IP3R = SR Ca release 4Ca:CAM
DAG activates PKC
PKC activates LTCC and inhibits K ch. (prevent repol)
4Ca:CAM activates MLCK (active myosin ATPase)
*a1:2 ratio sets contract/relax
2 (E) (Gs/Gi) - (Gs) relax blood vessels, uterus, bronchioles, eye
Activates AC (ATPcAMP), cAMP activates PKA
PKA inhibits MLCK and activates MLCP (ATPase
inactive; dephosphorylate myosin-P) relax
- (Gi) opposite of Gs; Inhibits AC contract

Contractile Cell (most)

Cond vel. = 0.3-0.5 m/s
AP dur. = Contraction dur. =
Atrial 200, Vent 300 ms
*Cant summate/tetanize dur. of
AP + conduction > contraction
duration
GENERAL CARDIAC CELL:
Striated, high ATP use ~ skeletal
Fairly small, electrically connected
thru gap junctions (intercalated
disks) ~ smooth
SYMP
1 (E, NE) (Gs)
Activates AC
cAMP activates PKA
PKA activates LTCC and RyR-2
PKA inactivates (phos) PLB =
unblocks SERCA-2
= intracellular Ca
== cont duration, cont strength

Nodal Fiber
Cond vel. = 0.2 m/s
Slow: delay b/t A and V
contraction allows LV
filling
Pacemakers
SA node 80 bpm
AV node - 45 bpm
Purkinje fibers - 35 bpm
*Conductive Fibers*
Cond vel. = 3-4 m/s
SYMP
1 (E, NE) (Gs)
Activates AC
cAMP activates PKA and If
(big Na in, small K out)
PKA activates LTCC
= Ph 4 slope
= VT
== HR (SA node)
=Ph 0 slope
== AV cond vel (AV node)
PARASYMP
m2AChR (Gi)
Inhibits AC
cAMP = PKA
= If, LTCC
& subunits activate
KACh ch. (repol, hyperpol)
= Vm
== HR
== AV conduction velocity
*block with Atropine

BIPN 105 Human Mammalian Physiology Lab Final Study Guide

Neuron
Depol: AP opens v-gated Na ch.
Time-gated Na ch. inactivation
Repol/Hyperpol: V-gated K ch.
activationV-gated K and Na ch.
deactivation
At Presynaptic Terminal: Depol
opens P/Q type Ca ch., Ca influx
ACh exocytosis (0.3 ms),
diffusion (0.05 ms),
activate nNAChR/nMAChR (0.15
ms) AP/EPP
ACH VESICLES
AChE: ACh = choline + acetate
Na/choline cotransporter:
choline and Na in
CAT (cholineacetyl transferase):
acetate + choline=ACh
VAChT (vesicle ACh
transporter): ACh into vesicles
SKELETAL MUSCLE
Resting Tone
PT = baseline b/t contractions
AT curve = top of a trapezoid

SR (using ATP)

LOCAL EFFECTS (90% local)

Exercise = CO2, pH, O2
== vasodilation in skeletal muscle blood vessels

Skeletal Muscle
FACILITATION
Residual Ca in presynaptic
terminal = ACh release

(Vascular) Smooth Muscle

1. Depol LTCC activate 100-300 ms = Ca plateau
Ca via SR and LTCC (most) 4Ca:CAM
Ca:CAM activates MLCK (activates myosin ATPase)

Contractile Cell (most)

0: PNa = fast depol = cond vel.
Then time-gated inactivation
*Na ch. blocker = cond vel.

2. Repol K ch. (4 types) activate

Ca inhibits LTCC and activates K ch. (repol)
K ch. inhibit LTCC too
Ca exits via NCX (3 Na in / 1 Ca out)
Ca returns to SR via SERCA-1 (using ATP)
MLCP inactivates myosin ATPase (dephos. myosin)

1: PNa, small PK = small repol

AP activates LTCC = PCa (30%)
LTCC activates RyR-2 to release
SR Ca (70%)
*frog: most Ca from outside

*Edrophonium (AChE blocker)

Constant nMAChR activation by
ACh in cleft = depolarization
blockade: Na ch. activate,
inactivate (time dependent), but
NO repol so cant deactivate
== muscle desensitized to ACh;
fatigue ability unchanged, but
there is fatigue in NMJ

3. Slow Wave Depol at rest own pacemakers

(myogenic; vs. neurogenic skeletal); drifts back up
after repol
4. Spread no T-tubules, but signal can reach inside
small cells; gap junctions electrically connect smooth
muscle cells into single unit sheet

2: PCa (LTCC), PK; Balance =

Ca plateau
Ca exits via NCX (3 Na in)
Ca reenters SR via SERCA-2
PLB inhibits SERCA-2
*PLB controls fate of Ca
3: PCa (Ca:CAM), big PK =
quick repol = AP duration

Nodal Fiber
0: PCa = cond vel.
Slower kinetics
2: PCa (LTCC), PK;
Balance = Ca plateau
3: PCa (Ca:CAM), big PK =
quick repol = AP duration
4: Spontaneous depol via If
(big Na, small K force) and
some Ca ch.

SA NODE
Ph 4 slope
VT (activate LTCC sooner)
Vm
== HR

STRETCH-INDUCED CONTRACTIONS
Opens Na and/or Ca ch. = faster depol = frequency
4: constant Vrest = no cell
More Ca in cell = amplitude, duration
automaticity
SMOOTH MUSCLE
CARDIAC CONTRACTILE CELL
PT curve steeper than skeletal muscle (cardiac is stiffer)
Resting Tone
AT curve shallower, stops after upslope
PT = elastic elements + Ca-independent crossbridges
Amplitude, Duration, Frequency (innate), Resting Tone
(+) inotropic state (myofilament interaction ability) = contractility = AT curve (shift up)

BIPN 105 Human Mammalian Physiology Lab Final Study Guide

TT - Doesnt respond to stretch at
plateau

resting tone = less excited state

Cardiac Loop: (+) inotropic = SV, peak

(-) inotropic = SV = heart failure; drug to AL to compensate

*In Lab 5: we measured resting tone because since no y-int,

there is no PT resting tone
Plasticity - when piece of smooth muscle is stretched and held,
PT initially increases and then after a while decreases because
AP-independent crossbridges break and reset to reduce T

Constant TL: PL (stretch) = AL = longer contractions

Constant PL (stretch): AL = T to match TL / T = pure isometric (no stretch)
Diastole vent. relaxes when PLV<PLA (mitral/bc valve opens), LV fills; LA contracts
Systole vent. contracts when PLV>PLA (mitral/bc closes) then isovolumetric phase
When PLV>Paorta, aortic opens, LV contracts, blood is ejected
*Paorta fluctuates
PL/EDV = more filling = Vasoconstriction (a1) =venous return =filling P
HR = filling time (longer diastole) = SV (FrankStarlingLaw)
== P, SV (no inotropic change)

Glomerulus

Proximal Tubule

300 mOsm
(300mOsm cortex and medulla)
High Pc
High PK (tight jx
open)
[blood]=[Bowmans
space]

Reabsorption:
100% glu, aa, proteins
70% H2O (bulk), electrolytes
50% urea

*Overall filtrate:
like plasma with few
proteins
isosmotic to plasma

*Overall filtrate:
Volume by 70% (H2O)
[glu, aa, protein] = 0
[urea]
isosmotic to plasma

Thin Descending

<1200 mOsm
(300->600->1200
mOsm medulla)
High PH2O
Low PNa = 0

== H2O efflux

Thin
Ascending
Limb
<1200 mOsm
(medulla high
[urea, Na])
Low PH2O
High PNa

== Na efflux
*passively
follows
gradient

Thick Ascending
Limb

Distal Tubule

Collecting Duct

Start: 100 mOsm

End: 50 mOsm

Entering filtrate: MOST DILUTE

*most reabsorption occurs pre collecting duct
PH2O reabsorption thru Aq2
ADH = PH2O (into tissue) = [Osm]urine
Aldosterone - ENaC, pumps
==Na reabsorption, K (and H) secretion
*doesnt affect blood/urine volume or [Osm]
because water follows

Low PH2O

Loop of Henle
*Overall filtrate
Volume by 15%
(85-90% H2O reabs.)
Na reabsorption
[urea]
Dilute filtrate

*Overall filtrate:
Na reabsorption
More dilute

*Overall filtrate:
Volume (GFR 125 bladder 1 ml/min)
Na and urea reabsorption
K (and H) secretion

BIPN 105 Human Mammalian Physiology Lab Final Study Guide

GLOMERULUS

PROXIMAL TUBULE
NA

Reabsorption:
Filtrate blood
Secretion:
Blood filtrate
*blood usually comes
from peritubular
capillaries
GFR (glomerular
filtration rate) how
well kidneys work;
125 ml/min (blood to
kidney), fairly
constant

Apical side (from filtrate):

Na ch. - Na in
Tight jx. Na from apical->basolateral side
Basolateral side (to blood):
Na/K ATPase - 3Na out, 2K in
GLU
SGLT2 (Na-glu cotransporter)
uses Na gradient to bring glu and Na in
GLUT facilitated diffusion - glucose out
*aas are transported similarly to glu (GLUT, SGLT2)
PROTEINS
Apical: proteases break down proteins into aas
Basolateral: vesicle endo- then transcytosis
BICARBONATE
(and H+ SECRETION)
NHE (Na-H exchanger): Na+ gradient created by Na/K pumps
brings H+ out, H + HCO3- in filtrate = H2CO3
CA (carbonic anhydrase): H2CO3 CO2 + H2O
CO2 + H2O (in cell) = H2CO3 (in cell) H + HCO3= HCO3- exits == more H+ in filtrate = pH
H2O
High PH2O: Aq1, Tight jx (which are pretty loose)
*follows osmotic gradient
UREA
Moderate Purea some follows H2O thru tight jx.
Most gets left behind concentrated

THIN
ASCEND /
DESCEND
LIMBS
---->

THICK
ASCENDING
LIMB
(Na reabsorption)
NKCC (Na-K-Cl
cotransporter)
Na, K, Cl influx
Na/K ATPase
3Na out, 2K in

DISTAL TUBULE
(Na reabsorption)
NCC (Na-Cl
cotransporter)
Na and Cl in
Na/K ATPase
3Na out, 2K in

Lab 1
Sweep speed (time/div); increase sweep speed = more accurate data
DC couple straight lights; AC couple drifts to baseline
Lab 2
Lab 3
Lab 4
Lab 5
UTERUS SMOOTH MUSCLE Lab 6
STARLING Lab 7
Starling
HR measured
Ventricular volume measured by chamber heart is placed in
Tubes remove effects of feedback loops
Arterial Pressure (AL) measured
Starling Resister (TPR is adjusted total R LV pushes against)
CO measured in volume

COLLECTING DUCT
PRINCIPAL CELL
(Na reabsorption, K secretion)
ENaC (epithelial Na ch.) brings Na in from filtrate
K ch. - K out
Na/K ATPase - 3Na out, 2K in
(Gs) coupled R - ADH binds = AC = PKA = inserts Aq2 from
vesicle membrane to apical mem. = PH2O
BP or [OsM]blood = ADH (post. pit)
= V1 (Gq) vasoconstrict. = BP
= V2 (Gs) PH2O (Aq2) = [Osm]blood, BP (via BV)
BP (=AII) or [K]blood = Aldosterone
= K secretion
= Na reabsorption = BV
== BV
INTERCALATED CELL
(b/t principal cells)
K secretion indirectly causes H secretion
H/K ATPase pump - H out, K in
H ATPase - H out
UREA
High [urea] in filtrate (has been concentrated) some
reabsorption through urea ch.

BIPN 105 Human Mammalian Physiology Lab Final Study Guide

ECG Lab 8
Leads
Chest / Precordial (monopolar, not augmented)
V1 ICS4/RSB
V2 ICS4/LSB
V3 V4 ICS5/MCL
V5 V6 ICS6/90 down chest wall
Frontal / Limb
Monopolar (+): Augmented voltage right, left, femur (avR,avL,avF)
Bipolar: I (LA+, RA-) II (LL+, RA-), III (LL+, LA-)
Waves
P width < 0.1 sec
If wide = atrial disease or Na ch. blockers
QRS complex width < 0.09 sec
If wide = ventricular disease or contractile cell conduction problem
T size is concordant with QRS complex size
Segments
RR HR = 60/RR
PR atrial depol + AV conduction + His; 0.12-0.2 sec
QT vent. depol + repol; QT = HR; 0.35-0.44 sec
QTc (corrected value) = QT / sqrt(RR)
ST Ca plateau; elevated/depressed = heart attack
Arrhythmia (check P and QRS waves)
Sinus rhythm a QRS follows every P; normal 60-100 bpm, sinus tachycardia >100, sinus bradycardia <60bpm
AV blocks cant conduct from atria to vent
1 slow AV conduction (PR int, doesnt affect HR)
2 intermittent conduction; P:QRS ratio exists; atrial rate is too high (damage); e.g. P 100bpm, QRS 50 bpm = 2:1 2 AV block; healthy AV node: P 300bpm, QRS 150 bpm
3 no conduction; Purkinje fibers pace ventricles (no Purkinje in frogs); Stannius #2
FLUID BALANCE Lab 9
Artherosclerosis damaged small, stiff blood vessels; TPR, which decreases CO (to maintain CO, need to MAP, leading to high BP)
Lab 10
Lab 11
BLOOD PRESSURE Lab 12
Korolkov Sounds
S1 M and T valves close, high freq (Diaphragm); start of systole
Split one ventricle delayed = RBBB (right bundle branch block) or signal to RV is lagging (while LV signal is normal)
S2 A then P valve closes, high freq, normally split (Paorta >Ppulmonary artery); start of diastole
Wide split RBBB, delayed even more, pulmonic valve open longer
Narrow split pulmonary hypertension, Prv with drop below Pvalve sooner
S3 - ICS5/MCL; mitral valve opens, rapid LV filling (fluid overload due to high BV), low freq (bell); early diastole after IVR
S4 ICS5/MCL; atrial contraction, stiff ventricle (hypertrophy due to high BP), low freq; late diastole
Auscultations
M/BC valve - ICS5/MCL
T valve - ICS4/RSB
A valve - ICS2/RSB

BIPN 105 Human Mammalian Physiology Lab Final Study Guide

P (pulmonic) valve - ICS2/LSB
Murmur 1/6 (cardiologist), 2/6 (resident), 3 (intern), 4 (med stu), 5 (anyone), 6 (steth off chest)
Stenosis ejection murmur, forward flow, small/stiff valve, blood flows fast (loud) then slow (quiet)
Aortic/pulmonic stenosis systolic ejection murmur from S1 to S2 after short delay for IVC
Mitral/tricuspid stenosis 1. diastolic ejection murmur from S2 middle of diastole after short delay for IVR mitral opens, initial high flow (doesnt build up)
2. 2nd diastolic ejection murmur from middle of diastole to S1 atrial contraction
Insufficiency regurgitant murmur, backward flow, leaky valve, low consistent rumble
Mitral/tricuspid insufficiency systolic regurgitant murmur from S1 to S2
Aortic/pulmonic insufficiency diastolic regurgitant murmur from S2 to middle of S1
Paorta > Pvent, Paorta is dropping, Pvent is increasing less backwards force so murmur stops (extends to S1 if bad enough)
Mitral valve prolapse bends into LA; valve closes, but bulges into LA when full; mid-systolic click, more risk of bacteria affecting valve (prophylactic antibiotics)
Mitral insufficiency click is heard in middle of systole, regurgitant murmur goes from click to S2
Lab 13 - Kidney Function
What we did drink solutes that alter plasma osmolarity, measure changes in volume, pH, [glu], specific gravity
Setups (and why) for each section
Calculations
Drugs?
Physiology
Water, coke (caffeine), diet coke (caffeine), chips (sodium)
Measure: volume (normalized by size and time since last pee), pH, glucose, specific gravity (density measurement)
Equations
Starlings Equation
= K[(Pc+i) (c+Pi)] = forces into tissue forces into capillary = weight
Ohms Law
Q = P/R
CO (ml/min) = HR * SV (ml) = MAP / TPR
MAP = Paorta
TPR determined by arteriolar tone (mainly), , # of open capillaries
R = 8L / r4
Osmometer
H/H0 vs. 1/C
Hematocrit (Hct) = RBC Volume / Total Volume
Nernst Equation
Equilibrium Potential Eion
Membrane Potential Vm
Strength/Duration
Amplitude vs. Duration
Chronaxie the stimulus duration required when stimulus amplitude is 2x the rheobase
Rheobase min. stimulus needed to elicit the criterion sized CAP

BIPN 105 Human Mammalian Physiology Lab Final Study Guide