Muscle Physiology III Flashcards
Cardiac muscle cells
- Cylindric, branched cells
- AUTOMATICITY
- intercalated discs
Intercalated discs:Transverse components
➢ Fascia adherens
➢ Desmosomes
Intercalated discs-Lateral components
➢ Gap junctions
Cardiac muscle -Long Action Potential with long
Refractory Period.
No temporal summation
• No tetanic contraction
Cardiac muscle-GAP junctions
all cells are
interconnected
• No spatial summation
Starling law of the heart
the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction
inc. in Ca++=
CONTRACTION
T-tubule
extension of cell membrane into the cell
Contain Ca++
Voltage-gated L-type 1,4 dihydropyridine receptor
Open the channel when an action potential stimulates the receptor
Sarcoplasmic reticulum
Form DIAD
• Store Ca++
RyR-2
Is stimulated by Ca++
• Release Ca++ from SR
Calcium “spark”
calcium released by RyR from SR
as result of the Ca++
-induced Ca++ release “CICR”
what type o Ca++ is ESSENTIAL in cardiac muscle contraction
Extracellular Ca++
COMMON PATHWAY IN STRIATED MUSCLE CONTRACTION
Ca++ binds TROPONIN C TROPOMYOSIN moves away from myosin-binding
sites on the actin CROSSBRIDGE –muscle contraction
80% Ca++ reuptake into-
SR:
• SERCApump
20% Ca++ extruded into the-
extracellular fluid:
• Na+/Ca++ exchanger
• Ca++ATPase pump)
Thick filaments:
• MYOSIN II
Thin filaments:
ACTIN
• TROPONIN (only in striated muscle)
• TROPOMYOSIN
Regulatory protein–Striated muscle
TROPONIN
Regulatory proteins-Non-striated muscle
CALMODULIN
Inotropism
the ability of the myocardial cells to change the force/strength of contraction
at the level of the cell and this modification can occur independently of any change in
force caused by alterations in preload or afterload on the heart
Anrep effect
abrupt increase in afterload produces a modest increase in inotropy
Bowditch effect
(increase in heart rate produces a small (+) inotropic effect
Gs-protein linked receptors:
Stimulate muscle contractility
• Beta-1 receptors
Gi-protein linked receptors:
• M2 receptors
Gi-protein activation predominates in the SA node
and in the AV node where the activation produce
decrease Heart Rate and Conduction Velocity
Gq-Protein and IP3- Coupled
Signal Transduction
+) Inotropic Drugs–Beta agonists: Gs-Protein linked receptors
- Dopamine
- Dobutamine
- Epinephrine
(+) Inotropic Drugs-Milrinone
Phosphodiesterase inhibitors: increase cAMP
Digoxin
-Cardiac glycoside.
-Direct inhibition of Na+/K+ATPase,
-decreases the
gradient of Na+ and
-indirectly inhibits Na+/Ca++
exchanger
Clinical use-Digoxin
Systolic Heart
Failure
Smooth muscle
-Non-striated pattern NO SARCOMERE
-
Smooth muscle-Caveola
Analogue to T-tubule
Extracellular Ca++
Smooth muscle-Sarcoplasmic reticulum
Poor developed
Intracellular Ca++
Smooth muscle–Dense bodies
(α-actinin; analogous to Z-lines in striated muscles
-Intermediate filaments (desmin & vimentin)
Smooth muscle-Thin filaments
Actin + Caldesmon + Calponin + Tropomyosin Lack TROPONIN (regulation in striated muscle contraction)
Smooth muscle-Thick filaments
Myosin II
Smooth muscle-Actomyosin regulation
Thick filament: phosphorylation of the regulatory light chain of Myosin II (myosin-linked regulation) –Ca++/CaM mediated
Smooth muscle-muti eg.
Ciliary muscle of the eye
• Sphincter pupillae muscle
• Dilator pupillae muscle
• Piloerector muscles
