Ventricular action potential
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
| Cardiology Network |
 Discuss Ventricular action potential further in the WikiDoc Cardiology Network |
| Adult Congenital |
|---|
| Biomarkers |
| Cardiac Rehabilitation |
| Congestive Heart Failure |
| CT Angiography |
| Echocardiography |
| Electrophysiology |
| Cardiology General |
| Genetics |
| Health Economics |
| Hypertension |
| Interventional Cardiology |
| MRI |
| Nuclear Cardiology |
| Peripheral Arterial Disease |
| Prevention |
| Public Policy |
| Pulmonary Embolism |
| Stable Angina |
| Valvular Heart Disease |
| Vascular Medicine |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
At rest, the ventricular myocyte membrane potential is about -90 mV, which is close to the potassium reversal potential. When an action potential is generated, the membrane potential rises above this level in four distinct phases.
The beginning of the action potential, phase 1, specialized membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell. This causes the membrane potential to rise at a rate of about 300 V/s. As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation.
The sodium channel opening is followed by inactivation. Sodium inactivation comes with slowly inactivating Ca2+ channels at the same time as a few fast K+ channels open. There is a balance between the centrifugal flow of K+ and the centripetal flow of Ca2+ causing a plateau of length in variables. The delayed opening of more Ca2+-activated K+ channels, which are activated by build-up of Ca2+ in the sarcoplasm, while the Ca2+ channels close, ends the plateau. This leads to repolarisation.
The depolarization of the membrane allows calcium channels to open as well. As sodium channels close calcium provides current to maintain the potential around 10 mV. The plateau lasts on the order of 100 ms. At the time that calcium channels are getting activated, channels that mediate the transient outward potassium current open as well. This outward potassium current causes a small dip in membrane potential shortly after depolarization. This current is observed in human and dog action potentials, but not in guinea pig action potentials.
Repolarization is accomplished by channels that open slowly and are mostly activated at the end of the action potential (slow delayed-rectifier channels), and channels that open quickly but are inactivated until the end of the action potential (rapid delayed rectifier channels). Fast delayed rectifier channels open quickly but are shut by inactivation at high membrane potentials. As the membrane voltage begins to drop the channels recover from inactivation and carry current.
See also
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
