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Regulation of cardiac muscle contraction

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

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Regulation of cardiac muscle contraction

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  1. Regulation of cardiac muscle contraction • Graded contractions • Effect of cardiac muscle stretching • Channel activity during action potentials • In myocardial contractile cells • In autorhythmic pacemakers

  2. Graded contraction • The amount of force varies with the number of cross-bridges formed • Low Ca++ few cross-bridges • High Ca++ more cross-bridges

  3. 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

  4. 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

  5. Effect of phospholamban on Ca++ release • NE and E activity • increase phospholamban activity • increase Ca++ ATPase activity on SR • more Ca++ is sequestered into the SR • more Ca++ is available for Ca++ release during stimulation • stronger force of contraction

  6. Effect of NE and E on contraction • Stronger, more frequent contractions

  7. When myocardial cells elongate • The amount of Ca++ entering the myocardial cells may increase  the force of contraction increases

  8. 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

  9. Long action potential • Myocardial cell refractory period and contraction end simultaneously

  10. Action potentials in myocardial autorhythmic cells • The channels: • If channels allow passage of Na+ and K+ • Ca++ channels

  11. 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

  12. 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

  13. 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

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