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MG: circulatory tract for bachelor pharmacy RUG
alle college aantekeningen van MG: circulatory tract for bachelor pharmacy RUG
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Voorbeeld 4 van de 38 pagina's
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MG circulatory tract lecture notesArtery = away from the heart
vein = towards the heart
Coronary artery system – coronary flow only occurs
during diastole (relaxing)
- Heart; large metabolic need; but is poorly
perfused tissue (Angina, MI, heart failure)
Sinus node – provides electrical impulse that causes the
heart to contract
Sinoatrial (SA) node – cardiocytes (do not contract) =
leading pacemaker
- Depolarize due to unstable membrane potential
leading to ventricle contraction
- If SA is damaged, slower pacemaker cells take
over (e.g. AV node)
Cardiomyocytes: perform contractions of the heart (due
to Na influx)
Via A-V bundle (bundle of his) and Purkinje fiber →
electrical signal is transported over heart
SA node: depolarization 100 times/minute → resting heartbeat of ± 70 BPM
AV-node: 40-60 BPM
Purkinje fibers: 30-40 BPM
Refractory period (heart): After an action potential initiates, the cardiac cell cannot initiate
another action potential for some time. This period is referred to as the refractory period,
which is ~250ms in duration and helps protect the heart.
Longer refractory period in cardiac muscle fibers compared to skeletal muscle fibers
During polarization in cardiac muscle fiber → also contraction
happening (no tension build up what would exhaust the heart –
no accumulation of muscle tension)
Tetanus = muscle cramp (not occurring in cardiac muscle)
Skeletal muscel – voluntary movement (by somatic motor
neurons → release of ACh)
- Nicotinic receptors on the motor end plate → ligand-
gated ion channels
, - Due to sodium influx → action potential
- DHP open and activate RyR receptor → increased Ca2+ in the cell → binds troponin
→ muscle contraction
Restoring of membrane potential by: Na+/K+
ATPase and Na+/Ca2+ exchanger
Funny channels – pacemaker potential (Na+ influx
in cells)
Ca2+ channel – depolarization (threshold – CA2+
into cells)
K+ channel –
Know which ions are flowing during which part of the potential
• Pacemaker cells (cardiocytes) do not contract.
• The plateau phase is the main difference between the AP of pacemaker cells and the
AP of contractile cells.
• If (funny) sodium channels are responsible for the potential phase of the pacemaker
AP.
• Calcium channels are responsible for the rising phase of the pacemaker AP.
• Differences between pacemaker and contractile cell (cardiomyocyte): contractile cell
has sarcolemma, large intracellular calcium store, different ion channels (rapid
sodium channels) and AP initiates at -90 mV instead of -60 mV.
• Conduction of AP from one contractile cell to another contractile cell occurs via ion
flows through gap junctions → threshold AP -70 mV reached, rapid sodium channels
open
Contraction starts when Ca2+ enters
the cell (calcium-induced calcium
release)
autorhythmic myocardium = pacemaker cells
,skeletal muscle: tendon attachment
Sarcoplasmic reticulum → Ca2+ storage
Myofibril: bundle of contractile and elastic proteins
Sarcomere: interaction between myosin and actin
No overlap between actin and myosin filaments → no more
tension
stretch, pacemaker activity (ion channels) electrical stim. →
relaxation: inhibition of MLCK
- Activation of MLC phosphatase (dephosphorylation)
, Cardiac muscle cells
- Striated muscle, sarcomeres present, one nucleus per
cell
- Ca2+ induced contraction
Gap junctions: transmission of signals to/from neighboring
cells
Desmosome: contact between cells
T-tubule: conduction of action potential
Large sarcoplasmic reticulum for Ca2+ storage
Heart: autonomic because of autorhythmic cells, but is
regulated by the autonomic nervous system
No action potential generation
- Affects heart frequency, contractile strength and
conduction
Sympathetic stimulation and epinephrine depolarize autorhythmic cell and speed up the
depolarization rate which increases the heart rate
the cardiac effects of a β-
agonist are increased heart
rate, contractility, conduction
velocity, and relaxation rate
Parasympathetic stimulation hyperpolarizes the membrane potential of autorhythmic cell
and slow depolarization which decreases the heart rare
- Increase K+ permeability
- Reduced Ca2+ permeability
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