Neural control of cardiovascular system

Question 1

Darcys law and Poiseulles law ?

Answer 1

Question 2

Why is blood flow important (cardiovascular system?

Answer 2

-Oxygen delivery
-Co2/metabolite removal
-Temperature regulation

Question 3

What is diffusion time proportional to?

Answer 3

Distance^2

Question 4

Describe how blood flow depends on pressure and resistance.

Answer 4

> Darcys law of flow
-Q, Volume of blood transferred per unit time (ml/min) = ΔP/R

-Flow is directly proportional to pressure and inversely proportional to resistance

Question 5

What factors influence blood pressure?

Answer 5

1. Pump more blood
   >Increases HR/SV = cardiac output
   >Increase force of contraction
2. Constrict tubes
   >Vasoconstriction - increases total peripheral resistance

Question 6

Blood pressure:
1.What is blood pressure
1.a - What is pulse pressure
2.How to calculate Mean arterial blood pressure?
3. What is arterial blood pressure normally expressed as?

Answer 6

1.Force exerted by blood on the vessel wall during the cardiac cycle
1.a. Systolic pressure - diastolic pressure
2. DBP + PP/3
3. Systolic/diastolic 120/80 mmHg

Question 7

How is ABP at larger arteries maintained during diastole to 80mmHg?

Answer 7

1.Arteries are highly distensible as they contain elastin which stores lots of mechanical energy
2.During systole when blood is ejected from ventricle into arterial system, the elastic arteries stretch allowing them to act as a temporary storage vessel for blood and mechanical energy
3. During diastole when ventricular pressure drops, elastic fibres allow vessels to recoil, which pushes blood through vessels

→ Maintain diastolic pressure so it doesn’t drop too low
→ Continuous blood flow during diastole as well as systole

Question 8

Why does systolic blood pressure increase with age?

Answer 8

• arterial compliance decreases with age, which leads to arterial stiffening

Question 9

We have a tight regulation of ABP? What happens if it gets too high or too low?

Answer 9

High:
- increase wall tension increased vessel radius
> lead to aneurysm.. rupture

Low:
1. Reduced blood pressure to vital organs
2. Reduced O2/nutrient delivery to organs
3. Organ dysfunction
- Can lead to dizziness

Question 10

Where are arterial baroreceptors found?

Answer 10

Question 11

How do baroreceptors work?

Answer 11

-Transient Receptor Potential Channels open in response to stretch
–High BP (baroreceptors stretched)
-Increase entry of ions = depolarisation
» activate nerve , increase firing rate of CN

Question 12

Describe the baroreflex of and increase in blood pressure.

Answer 12

Question 13

1. What is HR determined by?
2. How does AP from the SA nodal myocyte especially differ from atrial and ventricular myocyte?

Answer 13

1. Rate of decay of pacemaker potential
   > Steeper slope → faster HR
2. SA nodal myocytes are able to spontaneously depolarise without having to receive AP

Question 14

What are the parasympathetic and sympathetic effector mechanisms?

Answer 14

-PARASYMPATHETIC: decrease HR
-SYMPATHETIC: increase HR, myocardial contraction, peripheral vasoconstriction

Question 15

Heart rate is controlled by the autonomic nervous system.
How?
(Chronotropy)

Answer 15

SYMPATHETIC:
> adrenaline or noradrenaline are released from post ganglionic sympathetic neurones onto SA nodal myocytes
1. Binds to beta 1 ARs which are Gs linked metabotropic receptors
2. Activation of AC by Gs subunit
3. Increased concentration of 2nd messengers cAMP
4. Increased cAMP concentration modulates gating properties of HCN by increasing its probability of it opening, which leads to influx of Na+
5. This leads to increased funny current, leading to increased rate of decay of pacemaker potential
6. Membrane potential reaches threshold for AP generation quicker so more AP can fit in per unit time to increase HR

PARASYMPATHETIC:
1. ACh binds and activates M2-AChR on SA nodal myocytes which are Gi linked metabotropic receptors
2. This leads to inhibition of AC by Gi subunit, decreasing cAMP concentration
3. This decreases opening probability of HCN channel, reducing funny current
4. Rate of decay of pacemaker potential decreases, so longer for membrane potential to reach threshold for AP generation, resulting in decreased HR

Question 16

How does the sympathetic nervous system modulate EC-Coupling ?
(Ionotropy)

Answer 16

> Ventricular myocyte
1. A/NA bind to b1 adrenergic receptor > Gs stimulation > ^cAMP > ^PKA > Phosphorylates….

2. PKA targets :
   - L-type Ca2+ channel = ^Ca2+ influx
   - Ryanodine receptor (RyR2 ) = ^Ca2+ fractional release
3. Increases the amount of calcium released into the cytoplasmic space > More binding to the myofilament > Increase force of contraction
4. Final target of PKA = Phospholamban (PLN) which acts as a brake on SERCA activity
   >Braking activity is reduced so increased SERCA activity > More calcium is taken back into the SR :
5. Increased rate of calcium intake → Increased rate of relaxation (lusitropy)
6. SR replenished with more calcium, increasing size of calcium store → More calcium available for release following next depolarisation/ heart beat, increasing force of contraction

Question 17

Important point “ a2/b2 adrenergic receptors are present in arterioles of different tissues. What does this result in?

Answer 17

-Different tissue = different specific effects

Question 18

How does the sympathetic tone modulate vasoconstriction?

Answer 18

1) Activates adrenal medulla to release NA which binds to a1-ADR
2) Gq dissociates from receptor and activates PLC > liberates IP3 + DAG from PIP2.
4) IP3 binds and opens IP3 receptors on surface Sarcoplasmic reticulum > releases Ca2+ from SR increase in cytosolic Ca2+
5) Ca2+ binds and activates enzyme CaM (calmodulin) > activates MLCK > increases phosphorylation of myosin heads > Vasoconstriction of arterioles