Lecture 32 Flashcards
T-tubules in skeletal muscle
A-I band intersection
T-tubules in cardiac muscles
in ventricles at Z-lines
Intercalated discs:
Desmosomes prevent cells from separating contraction.
- Contain gap junctions that allow the action potentials to be carried from one cell to the next
- Allows for the coordinated contraction of all the myocytes
Ventricular myocyte action potential
- Action potential is long lasting > 100 ms long
- Has plateau phase due to presence of a large sustained Ca2+ current (ICaL)
- Membrane potential depolarised throughout most of the twitch
The three major stages of an action potential in a cardiac muscle
- Rapid depolarisation due to fast voltage-gated Na+ channel
- Plataeu phase due to slow voltage gated Ca2+ channel (L-type Ca2+ channel)
- Repolarisation due to closing of Ca2+ channels and opening of K+ (outward) channels
LTCC:
L-type voltage gated calcium cahnnel (ICaL)
RyR
Ryanodine receptor (Calcium channel in sarcoplasmic reticulum)
NCX
Sodium/Calcium exchanger
NKA
Sodium/Potassium ATPase
Cardiac muscle: Excitation contraction coupling
- Depolarization opens Na+ channels in the sarcolemma.
- Ca2+ influx by a Na+/Ca2+ exchanger
- Ca2+ influx triggers opening of Ca2+ sensitive channels in the SR (RyRa), which liberates bursts of Ca2+
- Ca2+ influx triggers. The raised intracellular Ca2+ concentration allows Ca2+ to bind to troponin, which then switches on the contractile machinery.
For relaxation to occur ___
Ca2+ must decline, allowing Ca2+ to dissociate from troponin. This requires Ca2+ transport out of the cytosol by four pathways:
- SR Ca2+ ATPase
- Sarcolemmal Na+/Ca2+ exchange
- Sarcolemmal Ca2+ ATPase
- Mitochondrial Ca2+ uniport
Ca2+ can exit the cytosol by four pathways:
- SR Ca2+ ATPase
- Sarcolemmal Na+/Ca2+ exchange
- Sarcolemmal Ca2+ ATPase
- Mitochondrial Ca2+ uniport
Trigger for Ca2+ release from SR in skeletal muscle
-Na+ influx
Trigger for Ca2+ release from SR in cardiac muscle
-Ca2+ influx
Heart rate is set by:
The pacemaker cells in the sinoatrial node. The rate can then be modified, especially via the autonomic nerves releasing neurotransmitters
Stroke volume is increased by:
Increased rate of firing
- Increasing stretch of ventricles
- Certain neurotransmitters
Pacemaker cells
- Unstable resting membrane potential
- Depolarization due to relatively slow Ca2+ current (not fast Na+)
Autonomic innervation of the heart
The vagus nerve decreases heart rate. Release ACh.
Sympathetic cardiac nerves
increase heart rate and force of contraction (release noradrenaline).
Increasing heart rate also increases:
contractile force
Starlings law of the heart:
-As the resting ventricular volume is increased the force of the contraction is increased.
Noradrenaline acting on B receptors and via second messengers acts on:
L-type channels resulting in more calcium entering the cell.
- Ca2+ pump in SR so SR increases its Ca2+ stores.
- Net result: bigger/shorter concentration
Noradrenaline released by sympathetic nerves leads to increased cytosol calcium
Due to increased HR shortening time for extrusion
