Regulation of cardiac muscle contraction • Graded contractions • Effect of cardiac muscle stretching • Channel activity during action potentials – In myocardial contractile cells – In autorhythmic pacemakers
Jan 14, 2016
Regulation of cardiac muscle contraction
• Graded contractions
• Effect of cardiac muscle stretching
• Channel activity during action potentials– In myocardial contractile cells– In autorhythmic pacemakers
Graded contraction
• The amount of force varies with the number of cross-bridges formed
• Low Ca++ few cross-bridges
• High Ca++ more cross-bridges
The effect of epinephrine and norepinephrine of contraction
• NE and E bind to beta 1 receptors on contractile myocardial cells
• The beta 1 receptor is coupled to a G protein
• Cyclic AMP is formed
The effect of epinephrine and norepinephrine of contraction
• cyclic AMP is formed
• 1. Voltage gated Ca++ channels are phosphorylated stay open longer more intracellular Ca++ stronger contractions
• 2. A regulatory protein, phospholamban, is phosphorylated increased activity on SR Ca++ ATPase contractions shorten duration
Effect of phospholamban on Ca++ release
• NE and E activityincrease phospholamban activity increase Ca++ ATPase activity on SRmore Ca++ is sequestered into the SRmore Ca++ is available for Ca++ release
during stimulationstronger force of contraction
Effect of NE and E on contraction
• Stronger, more frequent contractions
When myocardial cells elongate
• The amount of Ca++ entering the myocardial cells may increase
the force of contraction increases
Myocardial contractile cell action potentials
• Resting potential is stable -90 mV• Wave of depolarization through gap
junctions• Voltage gated Na+ channels open• Voltage gated K+ channels open• Slow voltage gated Ca++ channels open
and K+ channels close• Ca++ channels close and K+ channels
open
Long action potential
• Myocardial cell refractory period and contraction end simultaneously
Action potentials in myocardial autorhythmic cells
• The channels:– If channels allow passage of Na+ and K+
– Ca++ channels
Action potentials in myocardial autorhythmic cells
• Unstable resting membrane potential• Pacemaker potential• At a membrane potential of -60 mV Na+
enters through the If channels mb depolarizes Ca++ channels open Ca++ channels close K+ leaves
Modulation of autorhythmic cells
• NE (sympathetic) and E (adrenal hormone)
• Autorhythmic cells have beta1 receptors• Cyclic AMP levels increase• Properties of If and Ca++ channels altered• More rapid Na+ and Ca++ entry• Rapid action potential• Rapid contractions
Modulation of autorhythmic cells
• Parasympathetic, acetyl choline
• Muscarinic receptors
• K+ channels open mb hyperpolarizes cell less excitable
• Ca++ channel less likely to open slower depolarization cell is less excitable