Week 08 Lect 1 - Circulatory Regulation: Local Reg & Hormones (Dustin) Flashcards
What is the O2 content in the arterial supply?
Venous supply?
So what is the average arteriovenous O2 difference (AVDO2)?
Arterial: 200 mL/L
Venous: 150 mL/L
AVDO2 = 200 - 150 = 50mL/L
What are the 3 mechanisms of circulatory system control?
- Local Control (main topic of lecture)
- Hormonal/Humoral Regulation (slow process)
- Reflex Regulation (CNS involved)
What is the Bayliss Effect?
What is the (general) sequence of events in this effect?
Autoregulation involving myogenic tone,
characteristic of small arteries & arterioles
With a decrease in pressure, you would normally expect flow to decrease.
However, here the vessel musculature relaxes, vessel radius increases, so resistance goes down, which means flow is maintained/autoregulated
(the opposite happens with increase in pressure)
What specific changes occur in Bayliss effect during an increase in pressure?
Pressure increases -> tension on wall increases
- > mechanosensitive cation channels open
- > depolarization
- > L-type Calcium channels open
- > [Ca2+] increases
–> Vasoconstriction
Also, Transient Receptor Potential (TRP) Channels open
–> additional increase in [Ca2+]
What does the graph for the effect of metabolism on blood flow look like?
Beyond the normal level, metabolism increases with blood flow roughly linearly
What kind of control do the precapillary sphincter and smooth muscle of laminal arterioles/metarterioles get?
They don’t have any sympathetic innervation,
so they get local control
What is the general sequence of events when cell function is increased in regards to circulatory regulation?
(referring to when a cell starts working harder to perform a task)
Cell function increases -> metabolism increases
-> metabolite concentrations increase
–> vasodilation
What are the common local changes in metabolite concentrations that occurs during increased cell function?
Increased cell function leads to…
- pO2 decrease
- pCO2 increase
- lactic acid concentration increase / pH decrease
- adenosine increase
- [Potassium] increase
What is the name for when increased metabolite concentrations during high cellular activity leads to blood vessel dilation and increased flow?
Functional Hyperemia
(may be called Metabolic or Active Hyperemia too)
What is reactive hyperemia?
Why does it occur?
When a vessel is cut off from circulation (as in clamping or some other blockage), but after some time flow is restored, flow will initially be increased proportionally to how long/severly the vessel was occluded
Occurs because of the local control of metabolites that built up during the time of occlusion, causing vasodilation. But when blood flow is restored and metabolites are returned to normal concentrations, the vasodilatory effect ends and flow goes back to normal
What are the endothelium-mediated regulators of vasodilation?
(considering local effects here)
Prostaglandin I2
Nitrous Oxide (NO)
What are the factors that lead to nitrous oxide production
What is the ultimate effect?
Metabolism increases -> local [metabolite] increases
- > Resistance of vessel decreases
- > local flow increases
- > Shear Stress
- > endothelial cells activate
- > Nitrous Oxide production increases
–> vasodilation
What occurs specifically with an increase in nitrous oxide?
[NO] increase -> [cGMP] increase
- > Protein Kinase G
- > Relaxation of smooth muscle
What are the chain of events that result from prostaglandin I2?
Prostaglandin I2 -> Gs activation
- > [cAMP] increase
- > Protein Kinase A
- > Relaxation of Smooth Muscle
What is retrograde vasodilation?
Propagation of vasodilation to upstream arterioles that are critical for regional flow
