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.


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.


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.

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