Muscle Physiology III Flashcards

1
Q

inc. Ca++ n the Myosin Light

Chain Kinase

A
-Myosin Light
Chain Kinase
activated
-phophoryte 
-CONTRACTION
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2
Q

Smooth muscle contraction -Myosin II:

A
  • 2 myosin heavy chain
  • 2 myosin light chains (MLC):
  • Essential MLC
  • Regulator MLC
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3
Q

Smooth muscle contraction component

A

Myosin light chain kinase (MLCK)
Myosin light chain phosphatase (MLCP)
Calmodulin (regulator of contraction; homologous of Troponin C)
Ca++ (activator of contraction)

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4
Q

Voltage-gated 1,4 dihydropyridine calcium channels

A

Electromechanical coupling

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5
Q

Ligand-gated calcium channels

A

Pharmacomechanical coupling

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6
Q

Stretch-activated calcium channels

A

Myogenic regulation in arterioles (microvascular resistance)

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7
Q

Leak calcium channels

A

Unregulated

Mechanical stretch promotes inward movement of Ca++

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8
Q

Ca++ channel bocer

A

-Inhibit voltage-dependent L-type calcium channels - Dec .muscle contractility

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9
Q

Dihydropyridine CCB

A

-Act on vascular smooth muscle
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine
Clinical use: Hypertension, prevention of cerebral vasospasm (nimodipine)

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10
Q

Non-dihydropyridine CCB

A

-Act on heart:
-Diltiazem, verapamil
Clinical use: atrial fibrillation

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11
Q

cAMP pathway

A

-Enhances Ca++
reuptake
-RELAXATION

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12
Q

Beta-2 receptors are Gs-protein coupled:

A

Bronchial smooth muscle relaxation (bronchodilation)
• Uterine smooth muscle relaxation during pregnancy
• Blood vessels relaxation (vasodilation) in the skeletal muscle

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13
Q

Albuterol, levalbuterol, salmeterol, salbutamol (inhalation)

A

Bronchial smooth muscle relaxation –Bronchodilation

Clinical use: Bronchial Asthma

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14
Q

Terbutaline

A

Uterine smooth muscle relaxation in pregnant women –Tocolysis
Clinical use: premature labor

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15
Q

milrinone

A
Selective PDE-3 inhibitor
Phosphodiesterase 3 (PDE-3) converts cAMP into AMP in cardiac and smooth muscle
-Clinical use: short-term use in acute decompensated Heart Failure
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16
Q

milrinone -In cardiomyocytes:

A

inc . cAMP - inc. Ca++ influx - inc. Inotropy and Chronotropy

17
Q

milrinone -In vascular smooth muscle

A

inc. cAMP – Inhibition of MLCK activity – General Vasodilation

18
Q
Nitric Oxide (NO)
pathway
A

-cGMP
-Open K+ channels:
hyperpolarization
-Inhibit Ca++ entry
-MLCP

19
Q

Nitrates

A

Increase Nitric Oxide in vascular smooth muscle
Dilate veins&raquo_space; arteries …… Decrease PRELOAD
Nitroglycerine, isosorbide denitrate, isosorbide mononitrate
Clinical use: angina, acute coronary syndrome

20
Q

Hydralazine

A

inc. cGMP –vascular smooth muscle relaxation
Dilate arterioles > veins …… Decrease AFTERLOAD
Clinical use: severe hypertension (acute treatment); safe during pregnancy

21
Q

Nitroprusside

A

inc. cGMP –vascular smooth muscle relaxation

22
Q

Ca++ RELEASE

A
  • CICR
  • IP3
  • Contraction
23
Q

mechanism o RELAXATION

A
  • dec. Ca++

- dec. MLCK activity

24
Q

mechanism o RELAXATION-Cell repolarization

A

Decrease influx of Ca++

25
mechanism o RELAXATION-Reuptake of Ca++ to the SR:
SERCA pump
26
mechanism o RELAXATION-Plasma Membrane Ca++ ATPase Pump
Promote Ca++ efflux
27
mechanism o RELAXATION-Na+/Ca++ exchange mechanism
Promote Ca++ efflux
28
Latch mechanism or state
ns its full force of contraction despite reduced amount of continuing excitation and lesser energy required for comparable sustained skeletal muscle contraction -Low ATP utilization • Lower Ca++ concentration requirements
29
Latch mechanism or state-Importance
can maintain prolonged tonic contraction in smooth muscle for hours with little use of energy
30
Latch mechanism or state-Cause (hypothesis):
myosin dephosphorylation while still attached to actin during the crossbridge cycle
31
Ca++ sensitization
Decrease MLCP activity – Increase MLC phosphorylation
32
Ca++ de-sensitization
Increase MLCP activity – Decrease MLC phosphorylation