Unit 2 Lecture 11: Sympathetic Influences on Vasculature Flashcards
What causes SNS activity to be mitigated when we need high muscle blood flow
- Beta-adrenergic receptors that reduce vasoconstriction
- Metabolites overiding sympathetic vasoconstriction (Active hyperemia)
How are Active Hyperemia and Sympathetic Vasoconstriction correlated?
Active Hyperemia > Sympathetic Vasoconstriction in exercising muscle
* One is a more potent stimulus and that causes it to vasodilate
Both are active at the same time but one is more potent that it overrides the other
Explain how Active Hyperemia > Sympathetic Vasoconstriction works here
- Skeletal muscle: Large increases in metabolic activity increases metabolite production and active hyperemia which is greater than sympathetic vasoconstriction inducing vasodilation
- Kidneys, liver, GI tract: These have drops in blood flow indicating increased SNS activity inducing vasoconstriction
There is no increase in metabolic activity to overcome vasoconstriction in the kidneys (no active hyperemia)
Why does the brain have no influence of the SNS on its blood flow?
- It’s regulated by flow auto-regulation (local control)
- Lacks alpha adrenergic receptors to react to norepinephrine produced by SNS to cause vasoconstriction (systemic control)
What happens to the arterioles when SNS activity is high during stress & what is blood flow like to the capillaries?
- You get high MAP due to increased CO and this actually leads to high resistance in the arterioles because they are vasconstricting
- High resistance (TPR) is due to SNS activity increasing NE release and therefore constriction
- Blood flow to capillaries is low (less blood to organ) & that decreases gas and nutrient exchange & reabsorption of fluid from organ into capillary is favoured
High TPR = High MAP
What happens to the arterioles when SNS activity is high when skeletal muscle is active & what is blood flow like to the capillaries?
- We know arterioles of skeletal muscle will vasodilate because of metabolite production
- MAP is low so that means TPR will be of low resistance
- Metabolites are more favoured than SNS
- Capillaries will get more blood flow so better exchange of nutrients and gases and flitration from capillary to organ is favoured
MAP is typically high in exercise but in such circumstances where we have low TPR will have an effect on lowering MAP
If there is no local metabolic activity in an organ what does that encourage?
Vasoconstriction to the organ
* Once again, if there is no metabolite production, increased SNS activity takes over and vasoconstricts which we know decreases muscle blood flow
What is helping to regulate TPR in organs?
Both local and systemic even though local does not care as much as systemic they both still play a role nevertheless in regulating TPR
What is TPR ultimately affected by?
Arteriolar Radius and Blood Viscosity
- Arteriolar radius is affected by local and systemic control of blood flow (vasodilate/constrict)
- Thicker blood viscosity increases TPR and this increases MAP but we don’t want that as it leads to vasoconstriction
What local control factors affect arteriolar radius?
- Local metabolic activity (active hyperemia) (MAJOR FACTOR)
- Shear stress response which is caused by increased friction of blood from touching endothelial cells
- Flow auto-regulation (response to stretch)
- Heat-cold application (Blood flow increases to skin when heat is applied because active hyperemia increases metabolic activity of cells)
- Histamine release (increased blood flow due to histamine response from injury makes it regulator of blood flow locally)
What systemic factors of blood flow affect arteriolar radius?
- SNS activity
- Epinephrine and norepinephrine reinforcing SNS activity
- Angiotensin II and Vasopressin (hormones in fluid balance which exert vasoconstriction)
Where do capillaries branch from and where do they empty into?
Capillaries branch from smallest terminal arterioles and they empty blood into venules
Primary site of gas, nutrient and waste and water exchange
How big are capillaries?
The same size as RBC which is why they allow for movement of one RBC at a time
Why is the pressure dropping in capillaries but not 0?
We need a pressure gradient to allow for diffusion of nutrients and gases; pressure is from 20-40mmHG
Why is the capillary known for “form fitting function?”
- Thin wall allows for short diffusion distance of gases to where they need to go
Explain the capillary network
- When we branch off more the total cross sectional area increases and is the greatest at the capillaries
- The more networking we have, the more surface area we have to attain very efficient gas and nutrient exchange
- Blood velocity however slows down as we branch off more because there is greater SA so the blood does not flow as quickly in the capillaries
What is going on in this picture?
- Exchange of nutrients going through endothelial cells into organ
- Substances going to endothelial cell have to go through interstitial fluid through the capillary wall to get to the endothelial cells of capillary
- Vice versa for substances like glucose and O2 coming from capillary wall
- Metabolic waste produces also go in reverse direction towards the endothelial cells of the capillary
Exchange requires diffusion gradients
* Different ways of transporting substances whether it be passive or through channels
