Investigation on the Effect of Extracellular Calcium Concentration on Cardiac Function in the Langendorff Perfused Rat Heart
The mechanism of heart contraction and relaxation (mechanical restitution) is the basic of cardiac functioning. This mechanical restitution is driven by calcium movement and concentrations. An increase in cystolic calcium concentration causes contraction in myocardium. Calcium from the extracellular fluid enters the cardiomyocyte through the L-type Ca2+ channels after being propagated by the cardiac action potential which depolarises the cell. This flood of calcium triggers more calcium release from the sarcoplasmic reticulum via Calcium-Induced Calcium Release (CICR). Calcium binds to the ryanodine receptor on the sarcoplasmic reticulum which then causes vast release of more calcium. This calcium then forms cross-bridges by binding to the troponin.
Calcium binds to tropinin-C to induce a conformational change which moves tropinin-I away from actin/tropomyosin. Tropomyosin then moves to clear the myosin binding site on the actin thus allowing cross bridge attachment. Hence, contraction is critically dependent on intracellular calcium concentrations.
The process of cross-bridges formation and the shortening of the individual cardiomyocyte require ATP (phosphate group). The result of the shortening is contraction when the myosin heads swivel along the actin filaments of the cardiomyocytes. The greater the cystolic calcium concentration the greater the force of contraction as the calcium can bind to more tropinin-C. In cardiac muscle, the amount of calcium that is normally released from the sarcoplasmic reticulum alone is not enough to saturate all of the troponin sites. Hence, an increase in intracellular calcium means that more calcium will bind to more tropinin-C and more cross-bridges will be formed, causing an increase in contractile force. Based on this background, I hypothesise that an increase in the extracellular calcium concentration will lead to an increase in left ventricular pressure due to greater amount of cross-bridges, and an increase in
Calcium binds to tropinin-C to induce a conformational change which moves tropinin-I away from actin/tropomyosin. Tropomyosin then moves to clear the myosin binding site on the actin thus allowing cross bridge attachment. Hence, contraction is critically dependent on intracellular calcium concentrations.
The process of cross-bridges formation and the shortening of the individual cardiomyocyte require ATP (phosphate group). The result of the shortening is contraction when the myosin heads swivel along the actin filaments of the cardiomyocytes. The greater the cystolic calcium concentration the greater the force of contraction as the calcium can bind to more tropinin-C. In cardiac muscle, the amount of calcium that is normally released from the sarcoplasmic reticulum alone is not enough to saturate all of the troponin sites. Hence, an increase in intracellular calcium means that more calcium will bind to more tropinin-C and more cross-bridges will be formed, causing an increase in contractile force. Based on this background, I hypothesise that an increase in the extracellular calcium concentration will lead to an increase in left ventricular pressure due to greater amount of cross-bridges, and an increase in
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