Unit 2 Lecture 10: Regulation of Blood Flow Flashcards
What are the two ways to regulate blood flow?
- Local
- Systemic
What is local blood flow? What is systemic blood flow?
- Local: Originate in specific tissue; ensure a specific organ receives the blood flow it wants
- Systemic: Originate CENTRALLY; Mainly to regulate MAP
NOTE: In systemic, when blood is flowing to a organ from the system the control of blood flow happens externally not within the tissue itself because that would be local not systemic
Is local blood flow dependant on nerves?
Although local blood flow is signals within an organ controlling flow of blood, it is not dependant on nerves or circulating hormones
Those have to do with systemic control of blood flow (nerves and hormones)
What is the feedback loop used in regulating local blood flow?
- Active Hyperemia & Reactive Hyperemia
- Flow Auto-Regulation
What is Active Hyperemia and Reactive Hyperemia?
Hyperemia = increase in blood flow
* Both are driven by increase in metabolite production
* Metabolite production response may be due to local hormones not circulating
* Reactive = Requires blood flow restriction
* Active = Requires increase in metabolic activity
Increased ion fluxes detecting changes in O2, CO2
What are examples of locally generated hormones that we may see in local blood flow?
Nitric Oxide (smooth muscle) & endothelin are both local hormones (NOT SYSTEMIC CIRCULATING HORMONES)
Flow-auto regulation is a ________ dependant mechanism of smooth muscle cells?
Stretch
In Active Hyperemia when metabolite production in the tissue increases what happens to organ blood flow?
Increases
- Skeletal muscle is good because high exercise means high demand of blood flow
- Brain is interesting because only certain regions will respond to metabolic activity increase so blood flow increases in those regions (local blood flow)
Explain what the picture is showing?
When doing certain tasks, we have increase in metabolic activity for the certain areas of the brain doing the task which means organ blood flow will increase
Local blood flow will increase when metabolite production increases
Is this Active Hyperemia or Reactive Hyperemia?
This is Active as this is usually seen when you are actively increasing metabolic activity through exercise
- Increase in metabolites cause decrease in O2 production
- This leads to NO being produced and vasodilating the blood vessels and increasing blood flow
What is the negative feedback loop for Active Hyperemia once blood flow increases?
The increased blood flow actually acts as a negative feedback loop as it essentially brings back the concentration of O2 and decreases the metabolite production which will reduce the hyperemia stimuli
Remember hyperemia only occurs when O2 drops or when metabolite production increases
What is the difference between Reactive Hyperemia and Active Hyperemia?
Reactive as noted in the picture is due to lack of blood flow while Active is due to increased metabolic activity; INITIAL STIMULUS IS DIFFERENT
Explain how Reactive Hyperemia works when we cut off blood supply going to skeletal muscle for example
- Reducing blood flow (lack of blood) will accumulate more metabolites (anaerobic metabolism dependant) and reduce how much oxygen is circulating
- Once we stop cutting off blood flow, NO is stimulated to be produced and cause vasodilation to those vasoconstricted vessels and increase bloodflow
- Bloodflow then acts as a negative feedback loop by bringing back oxygen and signalling NO to stop being produced
In Coronary Blood Flow where do we have Reactive Hyperemia?
Initially we have constriction of blood flow in coronary arteries in systole (ventricular ejection) but reactive hyperemia acts during diastole to increase blood flow to coronary arteries
Where is Flow-Auto regulation very important in?
Kidney and Brain (Local blood flow)
- Organ blood flow remains constant no matter change in blood pressure
NOTE: In reality, it is a mix of both no auto and complete auto; when BP drops vessel vasodilates but it can’t for long as it can’t maintain constant blood flow (same with high BP and vasoconstriction ==> Can’t maintain constant blood flow)
Key Takeaway of Flow-Auto regulation?
It varies as it tries to vasodilate and vasoconstrict to specifically maintain a constant blood flow pattern
What causes Flow-Auto Regulation?
Myogenic response = Reflex response of arterioles to changes in blood pressure
Local negative feedback loop
Explain how myogenic response works with the figures below?
- When arterial pressure increases, there is a passive distension of arteriole wall
- Diameter of arteriole of A will increase due to need to stretch and this leads to increase in blood flow
- Active correction comes along in B which is the flow auto-regulation
- This brings the arteriole diameter down by vasoconstricting
- Stretch is flow auto-regulation which increases Ca2+ release into cytosol which increase contraction and strength of contraction & this reduces blood flow due to the constriction
This stretch (auto flow-regulation) actually leads to blood flow which initially increased from stretch to actually decrease as seen in the picture where B drops down
What unique properties of smooth muscle allow it to act as a flow auto-regulator (a.k.a stretch smooth muscle cell)
-
Stretch activated ion channels are activated upon stretch which activate Ca2+ ion channels (not seen in cardiac or skeletal)
* Depolarizes membrane upon stretch which enhances contraction of smooth muscle
Summary: Vasoconstriction and Vasodilation in Local Regulation are caused by?
- Vasoconstriction: Increased myogenic activity, Increased O2, Decreased CO2 and Metabolite production & Increased Endothelin
- Vasodilation: Decreased myogenic activity, Decreased O2, Increased CO2 & Metabolite production, & Increased Nitric Oxide
Two ways that Systemic Blood Flow is controlled?
- Neural: Sympathetic Nervous System
- Hormonal: Epinephrine, Angiotension II, Vasopressin
NOTE: PNS has no influence on blood vessels
Purpose: Regulates MAP
How does sympathetic neurons cause vasoconstriction?
Sympathetic neuron needs to be activated (stress, exercise, jumping in ice water bath) & this will release a hormone (Norepinephrine) which binds to the α-adrenergic receptor on smooth muscle
AP’s increase when Sympathetic neuron is activated
What receptors do the smooth muscle of arterioles & venules have?
α-adrenergic receptor
What receptors are in the arterioles of skeletal muscle?
β-adrenergic
β-adrenergic (predominant): Vasodilation
α-adrenergic: Vasoconstriction
What is unique about Epinephine, Norepinephrine and the two receptors?
- Norepinephrine has a stronger binding affinity to α-adrenergic receptors to cause vasoconstriction but it also binds to beta-receptors to cause vasodilation (beta-receptors known for dilating)
- Epinephrine has a stong binding affinity for β-adrenergic receptors which allows for vasodilation; however it can also bind to α-adrenergic to cause vasoconstriction
- Norepinephrine ==> α-adrenergic ==> Vasoconstriction
- Epinephrine ==> β-adrenergic ==> Vasodilation
- Norepinephrine ==> β-adrenergic ==> Vasodilation
- Epinephrine ==> α-adrenergic ==> Vasoconstriction
There are more α-adrenergic than β-adrenergic receptors. What does that mean for the arteriole?
More reactive to vasoconstriction than dilation
By activating β-adrenergic there is less vasoconstriction than if only α-adrenergic were active. What does this mean?
Since α-adrenergic are responsible for vasoconstricting, if those were only active, the arterioles would always be constricted but if we activate β-adrenergic receptors at the same time, not much vasoconstriction occurs
Where is epinephrine and norepinephrine produced from?
Norepinephrine: Sympathetic Neuron (SNS) at the arterioles
Epinephrine: Adrenal Medulla into the plasma