PHGY 214 Lecture Notes - Lecture 6: Antiporter, Lusitropy, Sodium-Calcium Exchanger
24 Jan 2017
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Document Summary
Channelopathy one of the most exciting area because we have cloned a different channel gens. We are able to transfect cells with channel genes into individual channels. It has been 50 years only in the 10 20 years we have a better understanding of the syndrome. Sodium channels 3 mutation in the genes responsible for the 90% of long qt patients. For the heart channel gene is her humans 400 different mutations identified. It is a common disease because sometimes, if there is a gene mutation, sometimes suffer from long qt syndrome. The process whereby an action potential triggers a myocyte to contract. Sinoatrial (sa) node 65 100 beats/min. Action potential starts and spreads all throughout the heart. Action potential generated from sinoatrial node and then through the pathway, depolarization will spread throughout the ventricles: describe the functional unit of contraction. Sarcomere basic contraction unit motor for contraction. Striations shown in skeletal and contractile cardiac muscles.
