Joanna Wieczorek

11/3/04
W8

Frog Heart Action Potential

Lab 9 Assignment

1. The atria contracts before the ventricle. This is demonstrated by the onset of the

AP in the atria while the ventricle is still in its diastolic state. Action potentials

show alternate firings of the atrium and the ventricle. Also, the atrial AP is

different in shape from the ventricular AP.i The amplitude of the AP is larger in

the ventricle than in the atria, and this corresponds to the higher forces needed to

circulate the blood into the systemic tubing.

2. A normal electrocardiogram is composed of a P wave which is caused by

electrical potentials generated as atria depolarizes prior to contraction, a QRS

complex which shows the depolarization wave spreading through the ventricles,

and a T wave caused by potentials generated as the ventricles recover from

depolarizationii. Before contraction, depolarization must occur through the

muscle. So, the P wave occurs right before atrial contraction and the QRS

appears before the contraction of the ventricles. The ventricles remain contracted

until after the T wave appears. By monitoring the EKG of the ventricle while

watching the AP at the atria, we could deduce certain relationships between EKG

recordings and action potentials. The AP appears in the atria just after the QRS

complex appears in the EKG. And the T wave appears just as the action potential

is ending.
3. The vagus nerve innervates the heart and upon stimulation will cause the release

of acetylcholine. Acetylcholine acts to decrease the rate of rhythm of the AV node

and to decrease the excitability of the AV junction fibers. Ach increases the cells

permeability to K+ and hyperpolarizes atrial cells. It also decreases the current of

Ca++. Therefore it makes it harder for a given stimulus to elicit a

response/contraction. Therefore, upon addition of acetylcholine, the time it takes

for an AP to spread to the ventricles in increased. So heart rate should slow and

the amplitude of the AP should decrease. We saw a definite decrease in amplitude

and a slight decrease in heart rate before our frog’s heart stopped during this

experiment necessitating epinephrine.

Atropine is a competitive antagonist of acetylcholine and therefore should reverse

the effects of vagal stimulation and cause heart rate and EKG recordings to return

to normal or make subsequent addition of acetylcholine less effective. The

presence of epinephrine in our frog’s heart makes it difficult to sort out the

changes made by atropine. Atropine occupies the acetylcholine receptors so after

adding more acetylcholine, the effects were not noticeable in terms of AP

amplitude, duration, or length of plateau.

4. Epinephrine is a neurotransmitter released by the sympathetic nervous system and

should increase heart rate. The addition of epinephrine is expected to increase the

levels of extracellular calcium and prolong the plateau period of the action

potential. It acts by increasing a nerve fiber’s permeability to sodium and calcium

ions. The increased Na and Ca cause the resting membrane potential to be closer

to threshold. The heart beats increase as less Na needs to come in before reaching
 threshold. The force of contraction should also increase due to extra Ca++ ions

near the myofibrils of the muscle. Addition of antagonists like prazosin (an alpha

receptor antagonist) and metroprolol (a beta receptor antagonist) will block any

further action of epinephrine. However, the antagonist will not display their own

effects on electrical activity of the heart.

5. High extracellular potassium levels will be toxic to the heart by rendering the

voltage across the membrane to be zero. Increasing extracellular K+ will

permanently change the relative charge inside the cell; at resting conditions there is a

-70 mV potential inside the cell relative to the outside. The different concentrations

of K+ on the inside and outside of the cell allow the cell to maintain an

electrochemical gradient. By increasing extracellular K+, the negative membrane

potential will be lost thus depolarizing the cell permanently. It will cause and

decrease in amplitude and frequency of action potentials until an action potential

simply cannot be maintained. The increase in K+ will ultimately kill our frog’s heart

by disabling electrical activity.

i
Yoshida, Shigeru. 2001. Simple Techniques suitable for student use to record action potentials from the frog heart.
Advances in Physiology Education 25, Page 7.
ii
Guyton and Hall. Textbook of Medical Physiology. 8th Edition. 1991. Page 118.