Muscle Physiology III Flashcards

1
Q

Cardiac muscle cells

A
  • Cylindric, branched cells
  • AUTOMATICITY
  • intercalated discs
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2
Q

Intercalated discs:Transverse components

A

➢ Fascia adherens

➢ Desmosomes

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3
Q

Intercalated discs-Lateral components

A

➢ Gap junctions

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4
Q

Cardiac muscle -Long Action Potential with long

Refractory Period.

A

No temporal summation

• No tetanic contraction

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5
Q

Cardiac muscle-GAP junctions

A

all cells are
interconnected
• No spatial summation

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6
Q

Starling law of the heart

A

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

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7
Q

inc. in Ca++=

A

CONTRACTION

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8
Q

T-tubule

A

extension of cell membrane into the cell

Contain Ca++

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9
Q

Voltage-gated L-type 1,4 dihydropyridine receptor

A

Open the channel when an action potential stimulates the receptor

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10
Q

Sarcoplasmic reticulum

A

Form DIAD

• Store Ca++

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11
Q

RyR-2

A

Is stimulated by Ca++

• Release Ca++ from SR

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12
Q

Calcium “spark”

A

calcium released by RyR from SR
as result of the Ca++
-induced Ca++ release “CICR”

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13
Q

what type o Ca++ is ESSENTIAL in cardiac muscle contraction

A

Extracellular Ca++

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14
Q

COMMON PATHWAY IN STRIATED MUSCLE CONTRACTION

A

Ca++ binds TROPONIN C TROPOMYOSIN moves away from myosin-binding
sites on the actin CROSSBRIDGE –muscle contraction

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15
Q

80% Ca++ reuptake into-

A

SR:

• SERCApump

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16
Q

20% Ca++ extruded into the-

A

extracellular fluid:
• Na+/Ca++ exchanger
• Ca++ATPase pump)

17
Q

Thick filaments:

A

• MYOSIN II

18
Q

Thin filaments:

A

ACTIN
• TROPONIN (only in striated muscle)
• TROPOMYOSIN

19
Q

Regulatory protein–Striated muscle

20
Q

Regulatory proteins-Non-striated muscle

A

CALMODULIN

21
Q

Inotropism

A

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

22
Q

Anrep effect

A

abrupt increase in afterload produces a modest increase in inotropy

23
Q

Bowditch effect

A

(increase in heart rate produces a small (+) inotropic effect

24
Q

Gs-protein linked receptors:

A

Stimulate muscle contractility

• Beta-1 receptors

25
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
26
Gq-Protein and IP3- Coupled
Signal Transduction
27
+) Inotropic Drugs--Beta agonists: Gs-Protein linked receptors
* Dopamine * Dobutamine * Epinephrine
28
(+) Inotropic Drugs-Milrinone
Phosphodiesterase inhibitors: increase cAMP
29
Digoxin
-Cardiac glycoside. -Direct inhibition of Na+/K+ATPase, -decreases the gradient of Na+ and -indirectly inhibits Na+/Ca++ exchanger
30
Clinical use-Digoxin
Systolic Heart | Failure
31
Smooth muscle
-Non-striated pattern NO SARCOMERE | -
32
Smooth muscle-Caveola
Analogue to T-tubule | Extracellular Ca++
33
Smooth muscle-Sarcoplasmic reticulum
Poor developed | Intracellular Ca++
34
Smooth muscle--Dense bodies
(α-actinin; analogous to Z-lines in striated muscles | -Intermediate filaments (desmin & vimentin)
35
Smooth muscle-Thin filaments
``` Actin + Caldesmon + Calponin + Tropomyosin Lack TROPONIN (regulation in striated muscle contraction) ```
36
Smooth muscle-Thick filaments
Myosin II
37
Smooth muscle-Actomyosin regulation
``` Thick filament: phosphorylation of the regulatory light chain of Myosin II (myosin-linked regulation) –Ca++/CaM mediated ```
38
Smooth muscle-muti eg.
Ciliary muscle of the eye • Sphincter pupillae muscle • Dilator pupillae muscle • Piloerector muscles