CAM201 Lecture Notes - Lecture 3: Atrioventricular Node, Depolarization, Electrochemical Gradient

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taupefly760

12 Jun 2018

School

University of Tasmania

Department

CAM

Course

CAM201

Professor

Bonnie Bereznicki

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Treatet of Arrhythias

Ion Exchange in Cardiac Muscle Cells

• Ion exchange changes electrical properties of cell, which increases/decreases

cell excitability

• Increasing excitability increases arrhythmia risk

• When voltage-gated calcium channels open, Ca2+ flows in, increasing

contractility, excitability, and automaticity

• Sodium flows in- increases excitability

• Potassium flows out- decreases excitability

Sodium-Potassium Pump

• Transporter protein

• Uses ATP to pump 2 K+ into the cell, and 3 Na+ out of the cell

Exchanger Pump

• Removes excess Ca2+ by using energy stored in electrochemical gradient of Na+

by allowing Na+ (3) to flow across the plasma membrane down its

concentration gradient in exchange for the counter-transport of Ca2+.

• The stored energy is used to pump 1 Ca2+ out of the cell

Cardiac Muscle Electrophysiology

Certain electrophysiological features of cardiac muscle distinguish it from other

excitable tissues:

• Pacemaker activity

• Absence of fast Na+ currents in SA and AV nodes, whereas slow inward Ca2+

currents initiates action potential

• Long action potential (plateau) and refractory period

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• Influx of Ca2+ during plateau

The long refractory period is protective from re-excitation during a heartbeat

Cardiac Action Potential

Phase 0- Rapid Depolarisation

• Voltage-gated Na+ channels open rapidly at threshold (~-70mV), causing Na+

influx

• This causes membrane depolarisation

• The channels are open only for a few milliseconds

Phase 1- Partial/Early Repolarisation

• Voltage-gated Na+ channels close- inactivation of inward Na+ current

• Additional K+ channels open briefly

• The membrane transiently repolarises

Phase 2- Plateau

• L-type voltage-gated Ca2+ channels open slowly, allowing the slow influx of Ca2+

ions

• There’s a small outward flow of K+

Phase 3- Repolarisation

• The Ca2+ channels close

• Large increase in outward K+ current

Phase 4- Pacemaker Potential

• Na+/K+ ATPase pumps pump Na+ out and K+ into the cell cardiomyocyte

• Inactivation of the Ca2+ channels wears off, and there’s a small inward current

during diastole

• When the membrane threshold potential is achieved, phase 0 is triggered again

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SA and AV Node Action Potential

Phase 0- Depolarisation

• Opening of voltage-gated Ca2+ channels causes depolarisation

Phase 3- Repolarisation

• Opening of voltage-gated K+ channels causes depolarisation

Phase 4- Spontaneous Depolarisation

• Funny currents occur due to hyperpolarisation-activated sodium channels in

the SA node

• This accounts for the SA node’s automaticity

Arrhythmia

• Abnormal site of impulse formation and/or pattern of conduction

• Arrhythmia classification:

− Site of origin of abnormality (atrial, junctional, ventricular)

− Heart rate- bradycardia or tachycardia

• Causes of arrhythmia:

− Ischaemia

− Fibrosis and damage to heart disrupts electrical balance

− Stress (increased SNS activity)

− Drugs

− Electrolyte imbalance

• Arrhythmias are common in patients who are:

− Treated with digoxin

− Under general anaesthesia

− Suffering from AMI

Class I Antiarrhythmic

• They are use-dependent Na+ channel blockers, and they selectively block:

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Document Summary

Ion exchange changes electrical properties of cell, which increases/decreases cell excitability. Increasing excitability increases arrhythmia risk: when voltage-gated calcium channels open, ca2+ flows in, increasing contractility, excitability, and automaticity, sodium flows in- increases excitability, potassium flows out- decreases excitability. Sodium-potassium pump: transporter protein, uses atp to pump 2 k+ into the cell, and 3 na+ out of the cell. The long refractory period is protective from re-excitation during a heartbeat. Phase 0- rapid depolarisation: voltage-gated na+ channels open rapidly at threshold (~-70mv), causing na+ influx, this causes membrane depolarisation, the channels are open only for a few milliseconds. Phase 1- partial/early repolarisation: voltage-gated na+ channels close- inactivation of inward na+ current, additional k+ channels open briefly, the membrane transiently repolarises. Phase 2- plateau: l-type voltage-gated ca2+ channels open slowly, allowing the slow influx of ca2+ ions, there"s a small outward flow of k+ Phase 3- repolarisation: the ca2+ channels close, large increase in outward k+ current.

Related Questions

6. Consider the presence of hemoglobin in the catheter bag. Whatsymptom would this loss of

hemoglobin most strongly and immediately be linked to in thepatient?

A. Loss of blood volume

B. Loss of heartbeat

C. Drop in blood oxygen saturation

D. Liver failure

When a neuron is stimulated, the area of the membrane at thepoint of stimulation becomes

more permeable to Na+. If a cell starts at resting potential(-70mv), and is then stimulated:

A. The membrane voltage will become < -70mV, because Na+will move OUT of the cell.

B. The membrane voltage will become > -70mV, because Na+will move OUT of the cell.

C. The membrane voltage will become < -70mV because Na+will move INTO the cell.

D. The membrane voltage will become > -70mV because Na+will move INTO the cell.

. At the peak of the action potential, the Na+ voltage-gatedchannels close, and K+ voltage-gated

channels open in response to the positive membrane potential.In order to return the cell to its

negative resting potential quickly:

A. K+ will diffuse along its concentration gradient INTO thecell.

B. K+ will diffuse along its concentration gradient OUT of thecell.

C. Na+ will reverse its direction of diffusion OUT of thecell.

D. The sodium-potassium pump will move Na+ OUT of the cell andK+ INTO the cell.

E. None of the above would return the cell to its negativeresting potential quickly.

You experiment with higher concentrations of toxin and findcases when the cell could not

repolarize at all or, if it began to repolarize, itimmediately depolarized again. This tells you that

the toxin:

A. Prevents voltage-gated K+ channels from opening.

B. Increases the speed that the Na+ ion channels open.

C. Prevents the Na+ ion channels from closing.

D. Makes the Na+ ion channels close too soon.

E. Doesn

lavenderclam549

1. The plasma membrane of rod and cone cells are

a) At resting potential in the dark and deploarized in thelight

b) At resting pootential in the dark and hyperpolarized in thelight

c) Depolarized in the dark and hyperpolarized in the light

d) Hyperpolarized in the dark and at resting potential in thelight

e) Hyperpolarized in the dark and depolarized in the light

2. The equilibrium potential of K+ ions in nerve cells is about-90mV. The membrane potential of a typical nerve cells at rist is-70mV. Therfore

a) Increasing the permeability of a resting neuronal membrane toK+ ions will increase the membrane potential (that is, make it morenegative, inside with respcect to outside)

b) In nerve cells at rest, there is a net diffusion of K+ ionsout of the cell

c) Increasing the membrane potential of a nerve cell would slowthe diffusion of K+ ions out of it.

d) K+ is not the only ion that is permeable at rest

e) All of the above

3. Which of the following is responsible for the replarizingphase of the action potential?

a) Voltage-gated Na+ channels are opened.

b) The Na+-K+ pump restores the ions to theri original restingstate.

c) The permeability to Na+ increases greatly.

d) ATPase destroys the energy supply that was maintaining theaction potential at its peak.

e) The permeability to K+ increases greatly while that to Na+decreases

4. The Relative refractory period of an axonm conincides withthe period of

a) Activation and inactivatioin of voltage-gated Na+channels

b) Increased Na+ flux into the cell

c) Increased K+ flux into the cell

d) Increased K+ flux out of the cell

e) Increased Na+ flux out of the cell

5. The plasma membranes of rod and cone cells are

a) At resting potential in the dark and epolarized in thelight

b) At resting potential in the dark and hyperpolarized in thelight

c) Depolarized in the dark and hyperoplarized in the light

d) Hyperpolarized in the dark and tat resing potential in thelight

e) Hyperpolarized in the dark and depolarized in the light

1. The plasma membrane of liver cells contains a glucose uniportthat transports glucose by facilitated diffusion. When the[glucose] is higher inside the liver cell than the [glucose]outside the liver cell, the glucose uniport will

A. couple the transport of glucose out of the cell to thehydrolysis of ATP

B. couple the transport of glucose into the cell to thehydrolysis of ATP

C. switch to a closed conformation, allowing no transport ofglucose

D. transport glucose out of the cell by passive transport

E. transport glucose in of the cell by passive transport

2. Unlike the positive charged ion shown in the middle diagramof figure 11-4B, K+ is higher in concentration inside the cell. Howwill the membrane potential of a cell at rest (shown in both themiddle and right-hand diagrams of Figure 11-4B) affect theelectrochemical gradient for K+?

A. The membrane potential will increase the electrochemicalgradient

B. The membrane potential will decrease the electrochemicalgradient

C. The membrane potential will have no effect on theelectrochemical gradient

3. Which of the following proteins carries out activetransport?

A. gluclose symport

B. Bacteriorhodopsin

C. ABC transporter

D. NA K pump

E. All of the above

4. Aquaporin will not transport Na+ ions because

A. Two asparagine residues in the channel prevent the passage ofNa+ ions by binding the oxygen of each water molecule as it passesby

B. Na+ ions are repelled by the positive charges at the entranceto the channel

C. Na+ ions cannot make contact with the carbonyl (C=O) groupson all four sides of the channel

D. The passage of Na+ ions is energetically unfavorable becauseone side of the channel is hydrophobic in nature

5. The acetylcholine receptor is different from other channelproteins we have discussed, such as the K+ leak channel,because

A. The acetylcholine channel is composed of a single polypeptiderather than multiple subunits

B. The acetylcholine channel transports Na+ ions against theconcentration gradient for sodium

C. The acetylcholine channel has a much smaller diameter thanother channel proteins

D. The acetylcholine channel transports ions with theirassociated shell of water molecules

E. The acetylcholine channel is always open, and never switchesto a closed conformation

6. After opening briefly along the axon of a neuron,voltage-gated ion channels switch to an inactivated conformationthat slowly returns to the original closed conformation of theprotein. This slow change in conformation, requiring about amillisecond, is important because

A. all of the ions that were transported across the membranewhen the ion channels were open must be actively transported backto the other side of the membrane, restoring the originalconcentration gradient, before the ion channels can open again

B. ATP hydrolysis is necessary to drive this energeticallyunfavorable change in conformation

C. it prevents the action potential from reversing direction andtraveling back toward the cell body of the neuron

D. the channel protein must be dephosphorylated in order tocomplete the transport process and return to the originalnonphosphorylated conformation

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CAM201 Lecture Notes - Lecture 3: Atrioventricular Node, Depolarization, Electrochemical Gradient

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