CV System Part II(6 pages)
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CV System Part II
- Lecture number:
- Lecture Note
- University of Southern California
- Bisc 307l - General Physiology
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BISC 307L 2nd Edition Lecture 25 Current Lecture Excitation-Contraction Coupling & Relaxation This is a magnified portion of a cardiac muscle fiber. The T-tubular system is not quite as extensive as it is in the skeletal muscle. Step 1: The red zone is an action potential in the plasma membrane, or sarcolemma, of the muscle fiber. The inward current of this AP is not only carried by sodium ions but also by calcium ions. Step 2: Ca ions coming through voltage gated Ca channels is going to bind to the Ryanodine receptor- channel and open it(step 3). So the coupling between membrane depolarization and opening of the ryanodine receptor is not mechanical like in skeletal muscles, but it’s actually Ca ions acting as secondary messengers. Step 4: Ca ions that previously were sequestered in the SR are released. That calcium triggers contraction. Step 5: Calcium from other sources contributes to the increase in intracellular Ca, which triggers filament sliding in the same way it would in skeletal muscles (binding to troponin, tropomyosin moves out of the way, cross bridge cycling, etc.). How much of the Ca that causes contraction comes out of the SR and how much comes out of the plasma membrane? About a 90/10 ratio, respectively. So everything happening on the left is what triggers contraction and couples excitation to contraction. On the right side of the figure is what triggers relaxation – removal of Ca from the sarcoplasm, so the concentration falls back down to the original very low levels. The mechanism of removal of Ca is the same as in skeletal muscles. Ca pumps in the membrane of the sarcoplasmic reticulum (step 8) resequesters the Ca. But there is an additional secondary mechanism, a Ca/3 Na antiport at the top(step 9), which couples the extrusion of Ca against the concentration gradient to the inward movement of 3 Na ions in the direction of its gradient. The Na that would otherwise accumulate inside is pumped out by Na/K pump. (step 10) Catecholamine Modulation of Contraction Catecholamines (norepi and epi) are part of the sympathetic response. They will increase cardiac output, the amount of blood the heart pumps out per unit time. The scheme below explains how a catecholamine binding to an adrenergic receptor results in a more forceful contraction and greater stroke volume. Increasing both of those is an important way in which epi and norepi increase cardiac output and blood pressure. Starting from the top. Catecholamines bind to beta 1 receptors in the plasma membrane of cardiac muscle fibers. This activates a cAMP mediated phosphorylation, a kinase A phosphorylation of two important target proteins inside the skeletal muscle. -First, are the voltage gated Ca channels in the membrane, which get phosphorylated on the cytoplasmic side, resulting in an increase in the mean open time of the channels.
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