Cardiac and Smooth Muscle Flashcards
Cardiac muscle is ‘quiescent’. What does this mean?
The muscle does not pulse unless it receives an electrical impulse from the sinoatrial node (SAN).
What is a sarcomere?
Unit of muscle (skeletal and cardiac). A-bands made up of myosin. I-band made up of actin.
Z-lines repeat every 2 microns.
What is the structure of cardiac muscle filaments?
Regular lattice.
One thick filament surrounded by a ring of thin filaments.
What is the sarcoplasmic reticulum?
A membrane bound structure in muscle cells which contain large concentrations of calcium ions.
What are T-tubules and what is their function?
T-tubules are infoldings of the plasma membrane. Their function is to carry action potentials down into the centre of the cell to ensure co-ordinated contraction.
What is the terminal cisterna?
Where the sarcoplasmic reticulum associate with the T-tubules.
Give one feature of cardiac muscle that allows it to never fatigue.
Contains many mitochondria.
How long does cardiac action potential last? How is this different to skeletal muscle?
200-400ms.
This is much longer than in skeletal muscle - ensure spatial summation cannot occur and the refractory period is long.
This prevents tetanisation (continuous contraction) of the cardiac muscle - prevent arrhythmias.
How does excitation cause a release of calcium in cardiac muscle? (5 steps)
Calcium-induced calcium release.
- AP travels down T-tubule to L-type (voltage-gated) Ca2+ channels.
- Ca2+ channels open, extracellular Ca2+ enters cell.
- Ca2+ binds to calcium release channels on the sarcoplasmic reticulum.
- Ca2+ released from sarcoplasmic reticulum.
- Ca2+ binds to muscle filaments to stimulate contraction.
Where does the calcium required for skeletal muscle contraction come from?
The sarcoplasmic reticulum only.
The calcium ion channels of the SR are voltage-gated in skeletal muscle.
Where does the calcium required for cardiac muscle contraction come from?
Extracellular and intracellular(from the sarcoplasmic reticulum).
Extracellular calcium activates calcium-release channels on the SR.
What is a DHP receptor?
Voltage-gated calcium ion channel in T-tubule membrane.
How does relaxation of cardiac muscle occur?
Ca2+ is reuptaken into the sarcoplasmic reticulum through ATP-driven ion pumps SERCA (sarcoplasmic reticulum calcium ATP-ase).
Na+/Ca+ exchanger pumps Ca2+ out of the cell.
How does Ca2+ stimulate contraction?
Binds to troponin C which moves tropomyosin away from actin, exposing myosin binding site.
What happens when Ca2+ binds to troponin C?
Tropomyosin moves away from the thin actin filament, exposing the myosin binding site.
What is the length tension relationship in skeletal muscle?
Up to a point, increased length = increased force.
Overstretching will cause damage, thus decrease force.
What is the length-tension relationship in cardiac muscle?
Increased length = Increased tension/force
This occurs as increasing sarcomere length increases Ca2+ sensitivity and maximal activated force.
What is the force-frequency relationship in cardiac muscle?
Increasing the rate of cardiac contraction increases tension.
Frequency increases > SR Ca2+ content increases > force of contraction increases
Where is smooth muscle located?
In the walls of hollow organs (stomach, intestines, bladder, blood vessels).
What nervous system innervates smooth muscle?
The autonomic nervous system.
What are contractions of the GI tract initiated by?
Pacemaker cells, the Interstitial Cells of Cajal.
Give five characteristic features of smooth muscle.
- Non-striated
- Elongated shape
- Presence of dense bodies which anchor actin filaments
- Sarcoplasmic reticulum
- Gap junctions between cells to allow current and small molecules to flow.
What are autocoids?
Physiologically active factor released by cells. Typically act locally and briefly on other cells.
What neurotransmitter do sympathetic nerves release to arteries?
Noradrenaline
Name an important vasoconstrictor.
Angiotensin II
How does vascular smooth muscle contraction occur? (7 steps)
- Noradrenaline/angiotensin II binds to α1 adrenergic receptor.
- G-protein is activated - activates phospholipase C.
- Phospholipase C converts PIP2 > DAG +IP3
- IP3 causes Ca2+ release from sarcoplasmic reticulum.
- DAG opens receptor-gated channels - Na+ and Ca2+ enter cell.
- Na+ influx causes membrane depolarisation - voltage-gated Ca2+ channels open on membrane.
- Ca2+ triggers contraction of smooth muscle.
What are the two main vasoconstrictors?
Noradrenaline and angiotensin II
Outline nitric oxide mediated vasodilation. (6 steps)
- Endothelial cells release nitric oxide.
- NO activates guanylate cyclase which converts GTP > cGMP.
- cGMP activates protein kinase G
- Protein kinase G opens K+ channels in membrane causing membrane hyperpolarisation.
- cGMP also activates SERCA and PMCA which pump Ca2+ out of the cytoplasm.
- cGMP causes calcium desensitisation.
How does cAMP act as a vasodilator?
When adrenaline binds to B1 receptors - cAMP is produced which acts as a vasodilator.
What is cross-bridge cycling in smooth muscle?
Myosin-phosphate binds to actin to form actin-myosin-phosphate complex which dessociates back to myosin-phosphate.
Slow cycling enables indefinate contraction.
How is phosphorylation important in smooth muscle contraction?
Myosin can only form a complex with actin when it has been phosphorylated. Myosin phosphtase removes phosphate.
What inhibits myosin-phosphatase? (promotes contraction)
Rho Kinase
- causes calcium sensitisation. Promotes contraction.
What activates myosin-phosphatase? (promotes relaxation)
Nitric oxide, via cGMP.
- causes calcium desensitisation.
What ion causes action potential upstroke in skeletal muscle?
Influx of Na+
What ion causes action potential upstroke in smooth muscle?
Ca2+
