BIOC33H3 Lecture Notes - Cardiac Muscle Cell, Adenylyl Cyclase, Stroke Volume
Document Summary
Stroke volume regulation: force of ventricular contraction, end-diastolic volume, afterload (blood pressure) The sympathetic nerve innervates a cardiac myocyte (muscle cell) by releasing noradrenaline by binding to receptors. This leads to the production of adenylyl cyclase which leads to the production of camp. camp activates pka which opens up ca2+ channels. This influx acts on the sr and triggers further release of ca2+ from the sr. an increase in ca2+ triggers contraction. Increase in cytosolic calcium leads to increase in the force of contraction. Circulating hormonal adrenaline has the same effect. Increase in intracellular [ca2+] in cardiac muscle cells: increased binding of ca2+ to troponin: more cross-bridge formation between the thick and thin filaments, increase in ca2+ permeability of the sarcoplasmic reticulum (ca2+- induced calcium release). Therefore, ventricular contractility is regulated simply by sympathetic input enhancing calcium influx into the cardiac myocytes which enhance contraction.