PHYS30001 Lecture Notes - Lecture 19: Protein Isoform, Cardiac Arrhythmia, Depolarization
Document Summary
Ecc in hypertrophy: activation changes control away from l-type channels but still get ca in. Normally positioned right next to ryr some uncoupling of sl ca-influx and sr ca release (l-type: sr release channel link) suppression of sr ca release. More ca coming in through t-type channels, which aren"t necessarily linked with ryr why t-channels? (t = tiny, transient, low threshold) possibly a way to take triggering. Reduced expression of sr ca atpase, na-ca/h exchangers levels goes up. Ecc in hypertrophy: relaxation changes delay in sr ca uptake (allows longer period of ca interaction with myofilaments, so don"t need fast isoform of myosin) Reliance on na-ca exchange for ca exit in relaxation (relaxation associated depolarisation, pushes cell into arrythmia risk) Na-h activation to deal with acid loading due to bigger cell. Heart always functions at ascending part of curve. Sns compensation can keep heart function normal for a while before decompensation/failure happens.
