lecture 15: regulation of heart function

Question 1

intrinsic regulation

Answer 1

results from normal functional characteristics
not on neural or hormonal regulation
Starling’s law of the heart
total tension curve as a straight line
heart can pump without nerves outside of body

Question 2

extrinsic regulation

Answer 2

involves neural and hormonal control (nervous and endocrine system)
maintain homeostasis
parasympathetic and sympathetic stimulation
from ANS innervating the heart

Question 3

parasympathetic stimulation

Answer 3

part of extrinsic regulation
tonic regulation
how fast action occurs/propagates is affected
supplied by the vagus nerve
decreases HR
ACh secreted (bind to m2AChR on heart)
slower depolarization

shallower phase 4—> hyperpolarized
—-longer to get to threshold
—-K leaving, more Na comes in through If channels to reach phase 4 threshold
shallower phase 0—–> depolarization longer, conduction velocity affected

Question 4

sympathetic stimulation

Answer 4

part of extrinsic regulation
supplied by cardiac nerves
increases HR and force of contraction
E and NE released

steep phase 0 and steep phase 4
more rapid depolarization

Question 5

parasympathetic cardiac innervation

Answer 5

vagus nerve innervates SA node and AV node
none innervating cardiac contractile cells of ventricles
innervating only the nodal cells
mainly affect HR and conduction velocity of AP

Question 6

sympathetic cardiac innervation

Answer 6

cardiac nerve innervates SA nodal cells and AV nodal cells and cardiac muscle in ventricles

Question 7

parasympathetic control on nodal cell

Answer 7

Gi
ACH binds to m2AChR
inhibits AC activity
decreases cAMP and PKA activity
1. decrease in funny current channels activity —-> decrease in phase 4 slope (pacemaker cells) —-> decrease in HR —> - chronotropic effect
—-affects the SA node
—–decrease amt of time for heart beats
2. increase K/ACh channel activity —-> hyperpolarizes
—–K going out
—–ACh initiated transduction pathway
3. decrease LTCC activity due to decrease in PKA —> decrease in phase 0
—– takes longer to depolarize
—-decrease in conduction velocity —-> - dromotropic effect
—–affects AV node

Question 8

sympathetic control on nodal cells

Answer 8

Gs
E or NE binds to Beta 1 receptor on membrane (in pacemaker cells of heart)
activates AC, alpha subunit of Gs drops GDP and binds GTP
increase in cAMP, increase in PKA
1. increase of If channel activity (panacurin channel) —-> increase in phase 4 slope
—–reaches Vt faster (threshold) —-> increase HR (SA node affected), more AP per unit time
—–+ chronotropic effect (SA node), increase in HR
2. increase in LTCC activity —-> increase in phase 0 slope, steeper than normal
—–increase in conduction velocity
—–+ dromotropic effect (AV node)

Question 9

chronotropic effect

Answer 9

related to time
effect on HR
frequency of contractions, depends on depolarization rate
ex: SA node depolarizes @ 80-100 depolarizations/minute and AV node is 40 depolarizations/minute
by the time AV nodal cells can spontaneously generate AP the signal from SA node has already arrived to AV node through internodal pathways —> cause depolarization
can be positive or negative

Question 10

positive chronotropic effect

Answer 10

sympathetic
increase HR
effects mainly on SA nodal cells, pacemaker of the heart
depolarize at faster rate (R ventricle)

Question 11

negative chronotropic effect

Answer 11

parasympathetic
effect mainly on SA node
decrease SA nodal cells depolarization as well as AV nodal cells
decrease SA nodal cells, increase AV nodal cells
ex: SA 70 dep/min, AV 25 dep/min

Question 12

dromotropic effect

Answer 12

effect on both SA and AV nodal cells
larger effect on AV nodal cells
effect on conduction velocity (delay of AP)
SA node depolarizes at faster rate than AV node
AV node has delay of AP (~100 ms)
AV has shallower phase 4 and phase 0 than SA
—–longer to get to threshold and depolarization, depolarization rate lower
slope of phase 0 changes with ANS change

Question 13

positive dromotropic effect

Answer 13

sympathetic
slope is steeper
more LTCC activated, depolarize faster
delay in AV node decreases
increase in conduction velocity

Question 14

negative dromotropic effect

Answer 14

parasympathetic
phase 0/slope is shallower
less LTCC activated
longer to depolarize
delay in AV node increases
decrease in conduction velocity

Question 15

sympathetic control on cardiac contractile cells

Answer 15

Gs
only innervated by sympathetic NS (parasympathetic only on AV and SA nodal cells)
E or NE binds to Beta 1 receptor on membrane
increase in activity of AC, increase cAMP and PKA activity

PKA phosphorylates things, decreases activity of PLB which tries to inhibit SERCA2

1. increase in RYR2 activity
2. increase in LTCC activity —-> Ca goes from ECF into the cell, activated RYR2 receptor
3. increase in SERCA2 activity —> sequesters more Ca, larger concentration gradient
   —–more Ca moves out of SR during next cardiac cycle
   —–larger inotropic effect
   —–decreases contraction duration —-> Lusitropy effect

increases in cytosolic Ca —-> form more crossbridges, have larger force of contraction
increase in contractility —-> + inotropic effect

Question 16

phospholamban

Answer 16

PLB
protein that inhibits the SERCA2 pump
in sympathetic control of cardiac contractile cells (Gs)
PKA removes this inhibition

Question 17

inotropic effect

Answer 17

related to contractility
cardiac contractile cells
amount of Ca you have in the cell
function of Ca interaction with contractile filaments
positive or negative

Question 18

positive inotropic effect

Answer 18

E, NE, and digitalis have these effects
sympathetic NS
increase in contractility
function of Ca in thene cytosol of the cell

Question 19

negative inotropic effect

Answer 19

decrease contractility

Question 20

parasympathetic “effect” on contractility

Answer 20

no innervation on cardiac contractile cells of ventricle
can INDIRECTLY affect contraction but is NOT an effect

parasympathetic —> = chronotropic effect —> decrease HR (contracting L ventricle less) —-> increase filling ventricular phase (more time in diastole/relaxation phase) —> increase in EDV (more time to put blood in) —-> increase in stretch —-> Frank-Starling Law —-> increase force of contraction

done due to chronotropic effect, NOT done directly

Question 21

Wiggers diagram and how SV and HR affect CO

Answer 21

LAST TWO PAGES OF NOTES
TAKE INTO CONSIDERATION FOR STUDYING