L9/10- Cardiac muscle Flashcards
cardiac muscle is also
striated
position of nuclei in cardiac cells
central (1 or 2 per cell)
feature of cardiac muscle cells
intercalated discs
intercalated discs
for electrical and mechanical coupling with adjacent cells- see
which protein is abundant in cardiac muscle
myoglobin- to ensure enough oxygen for abundant contractions
how is cardiac tissue similar to skeletal tissue
both striated and contraction mechanism similar
how is cardiac tissue diff to skeletal tissue
: nuclei are central not peripheral; sarcomere not as developed, no T-tubules in sarcoplasmic reticulum; one contractile cell type- cardiomyocyte, cardiomyocytes communicate through gap junctions (intercalated discs)
how cardiac tissue increases in size
hypertrophy and hyperplasia
hyperplasia
multiplication of cells
hypertrophy
enlargement of individual cells
which peptides are released during heart failure - atrial
ANP- atrial natriuretic peptide released by atria e.g. congestive heart failure
which peptides are released during heart failure- ventricular distension
BNP- brain-type natriuretic peptide released by ventricles
e.g. left ventricular hypertrophy
ANP and BNP mode of action
- Switches off RAAS
Reduce arterial pressure by decreasing blood volume and systemic vascular resistance
- Increase urine output
- Reduce BP
conducting system of the heart
- Action potential originate in the sinoatrial node (SAN)
- The action potential diffuses across the atria and travels to the Atrioventricular node (AV)
- APs travel slowly through the AV node to allow the atria to contract and empty blood into the ventricles
- The AP then passes quickly down the AV bundle to the apex of each ventricle
- AP are then carried by Purkunje fibres from the AV bundle to the ventricle walls
rapid conduction from the AV node to the ends of the Purkunje fibres allows
the ventricular muscles to contract in unison- providing a strong contraction.
however conduction is not as quick as
cardiomyocytes
- due to abundant glucagon which slows down conduction
- allows synchronicity
purkunjee fibres are
abundant in glycogen
- have spare myofibrils and extensive gap junctions
heart is stimulated by the
sympathetic nervous system
heart in inhibited by
parasympathetic NS
outline how contraction occurs
1) Action potentials traveling along the sarcolemma and down into the transverse tubule (T-tubule) system depolarize the cell membrane.
2) Voltage-sensitive dihydropyridine (DHP) receptors (L-type calcium channels) open to permit calcium entry into the cell during phase 2 of the action potential.
3) Calcium influx triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels (“ryanodine receptors”), and increases intracellular calcium concentration from about 10-7 to 10-5 M.
4) Free calcium binds to troponin-C (TN-C) that is part of the regulatory complex attached to the thin filaments. When calcium binds to the TN-C, this induces a conformational change in the regulatory complex such that troponin-I (TN-I) exposes a site on the actin molecule that is able to bind to the myosin ATPase located on the myosin head. This binding results in ATP hydrolysis that supplies energy for a conformational change to occur in the actin-myosin complex. The result of these changes is a movement (“ratcheting”) between the myosin heads and the actin, such that the actin and myosin filaments slide past each other thereby shortening the sarcomere length. Ratcheting cycles occur as long as the cytosolic calcium remains elevated.
5) At the end of phase 2, calcium entry into the cell slows and calcium is sequestered by the SR by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase), thus lowering the cytosolic calcium concentration and removing calcium from the TN-C. To a quantitatively smaller extent, cytosolic calcium is transported out of the cell by the sodium-calcium-exchange pump. Unbinding of calcium from TN-C induces a conformational change in the troponin complex leading, once again, to TN-I inhibition of the actin binding site. At the end of the cycle, a new ATP binds to the myosin head, displacing the ADP, and the initial sarcomere length is restored.
