Things to remember for Block 3 Flashcards
Heart Sympathetic Receptors and effects
Beta-1 Receptors - Increased Contractility and Heart rate
GPCR of Beta 1
Gs
Heart Parasympathetic Receptor and effect
Muscarinic receptor decrease heart rate
What receptor type dominates systemic vasculature?
Alpha 1 receptors which increase vasoconstriction
What GPCR is Alpha 1
Gq
What receptor dominates pulmonary arteries?
Beta 2 Receptors
What GPCR does the Beta 2 receptor undergo?
Gs
What second messenger does Gq use in smooth muscle?
IP3
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What second messenger does Gs use?
cAMP
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What second messenger does nitric oxide use?
cGMP
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cGMP Effector in smooth muscle
Inhibits L type Calcium Channels
Excitation of MLC-P Dephosphorization
Causes the cell to relax
cAMP Effector in vascular smooth muscle
PKA which phosphorylates MLCK into its inactive MLCK-P
MLC can not phosphorylate and therefore the cell relaxes
cAMP Effector in cardiac muscle
Increase activity of L type calcium channel increasing influx of calcium ions
IP3 Effector in smooth muscle
IP3 increases calcium secretion from the sarcoplasmic reticulum
Increases NCX activity
Causes vasoconstriction
Alpha - 1 Location, Agonist, GPCR, Secondary Messenger, Effect
Systemic Circulation, Norepinephrine, Gq, IP3, Vasoconstriction
Beta - 1 Location, Agonist, GPCR, Secondary Messenger, Effect
Heart, Norepinephrine, Gs,cAMP activates PKa which directly binds onto calcium channel (No MLCK), Increased Heart rate and contractility
Beta - 2 Location, Agonist, GPCR, Secondary Messenger, Effect
Pulmonary Vessels, Norepinephrine, Gs, cAMP inhibits MLCK, Vasodilation
Difference between the signal cascades of vessels vs. cardiac muscle
In cardiac muscle their is no MLCK so cAMP increases calcium influx via PKa.
In vascular muscle cAMP inhibits MLCK and causes vasorelaxation.
Role of Pka in the heart
Pka increases calcium influx into the heart and increases the calcium flow out of the sarcoplasmic reticulum
Pka also increases SERCA activity by phosphorylating Phospholamban to stop its inhibition of SERCA
More calcium can flow into the cell and remove itself from actin to increase the number of and strength of heart beats
What does DAG do
activates contraction PKC in both the heart and vasculature
Extra target of cGMP within vascular tissue
cGMP dependent Chloride channels
Vascular Chloride channels
Activated by cGMP or Calcium
Allows chlorine to flow out of the cell
Process of vasomotion
First contraction of smooth muscle followed by the release of NO -> GC-> cGMP -> Phosphorylate phospholamban to increase SERCA activity and reuptake calcium to relax the cell + Activate cGMP coupled Cl channels -> Cl- moves out of the smooth muscle cell and depolarizes the cell and through coupling with gap junction continues to depolarize the next cell
What kind of currents exist in non-Pacemaker cells vs. Pacemaker cells?
Fast Na channels
The Steps of Pacemaker Action Potentials
4 0 3
4 - Pre Threshold Depolarization
- Sodium influx slowly from If or “Funny” channels
0 - Threshold depolarization
- Calcium influx through voltage gated calcium channels
- Calcium channels begin to close overtime
3 - Repolarization
- Opening of K+ channels
The Steps of Non-Pacemaker Action Potential
4 0 1 2 3
4 - Equilibrium potential of -90
- Strong K+ current
- Ca and Na channels are mostly closed
0 - Fast Depolarization -70 Threshold
- Opening of Sodium Channels and rapid influx
- K+ channels start to close
1 - Initial Fast depolarization
- Opening of fast Ikto Channels
- Calcium channels open
2 - Plateau phase
- Continual Opening of the Calcium channel
- Prevents reinitiating of action potential
3 - Repolarization
- Delayed K channels trigger
- Ca channels begin to inactivate
