Local & Systemic Control of Circulation Mutafova Flashcards
What are 2 ways that you can alter blood flow? How does this relate to Ohm’s Law?
By changing the resistance or the pressure of the vasculature.
Q (blood flow) = P1-P2/R
When resistance increases what happens to blood flow?
Resistance increases & blood flow decreases.
What is the equation for determing the resistance?
R=8nl/piR^4
What happens to blood flow when the following occur?
Pressure difference increases
The radius of the blood vessel increases
The length of the vessel segment increases
The viscosity of the blood increases
Pressure increases–>Blood Flow increases
Radius of the blood vessel increases–>Blood flow increases
Length of the blood vessel segment increases–>Blood flow decreases
Viscosity of the blood increases–>Blood flow decreases
How does an increase in metabolism in a tissue or organ affect its blood flow?
It increases its blood flow. But just to meet its minimum requirements.
What are 4 regulatory mechanisms that can be used to alter blood flow?
Changing the heart pumping.
Changing the resistance of the vessels.
Changing the amt of blood pooled in the veins.
Changing the total extracellular fluid volume.
What is the idea of dual control of circulation in peripheral tissues?
The idea behind this is that you have intrinsic mechanisms that regulate blood flow (like the metabolites surrounding a tissue) & you have extrinsic mechanisms (like neural control). Although the intrinsic are very powerful for regulation, they are not enough & you still need extrinsic. The relative importance of these 2 mechanisms is different in different tissues.
Ex: Skin & Splanchnic: neural control is most important.
What are the 2 main categories of intrinsic mechanisms to regulation circulation?
Mechanism #1: Metabolic Release of Vasodilators Nutrient Deficiency in vascular smooth muscle naturally causes vasodilation as well. Mechanism #2: Myogenic Sudden Stretch Reduced Stretch
What are the 3 specific mechanisms that we should know for intrinsic regulation of flow?
Pressure Flow Autoregulation
Active Hyperemia
Reactive Hyperemia
What is Pressure Flow Autoregulation? What equation is it based on?
What category of intrinsic mechanisms does it fall into?
The idea is based on Q=deltaP/R.
It is that if you have a sudden increase in arterial pressure…you would naturally get an increase in blood flow.
However, if this is something that you want to control–>you can by increasing the resistance of the blood vessel. This gives constant flow.
Pressure rises & b/c of autoreg resistance will proportionally rise to maintain constant flow.
This is a myogenic mechanism. Sudden stretch–when the blood vessel feels the sudden stretch of increased pressure & blood flow it automatically constricts, increasing resistance.
T/F When you are exercising and all of a sudden less blood goes to your GI & more goes to your heart & muscles…this is an example of Pressure Flow Autoregulation.
False. This is not auto regulation. This has to do with overall homeostasis.
What are the limits to pressure flow auto regulation?
It can’t be maintained at pressures above 160mmHg (here the blood vessel is forced to dilate) or below 60 mmHg (here the blood vessel can’t dilate more than they are to compensate for this low of a pressure).
What is Active Hyperemia?
Increased blood flow in response to increased tissue activity.
Ex: what happens to certain tissues when you exercise.
What is Reactive Hyperemia?
This is increased blood flow in response to a sudden release of an occlusion. The blood flow goes beyond the normal limits after this release.
Ex: If the coronary branches of the heart were compressed & then released…they would experience reactive hyperemia & receive more blood flow than normal for a while.
What are the vasodilator metabolic theories?
W/o O2 & nutrients, vascular smooth muscle can’t contract.
In response:
Either a deficiency of O2 OR increased metabolism of a tissue causes the release of vasodilators.
Clearly, these tissues need more O2 & nutrients…they need more blood flow SO they dilate the blood vessels supplying them.
What are some vasodilator metabolites?
Think this through…
Low O2/High CO2
High Lactic Acid/Low pH (like skeletal muscle that needs more oxygen)
High Adenosine/HighPO4-/High ATP (high metabolism)
Increased Osmolarity (we’re secreting stuff b/c we’re doing stuff).
The Randos:
K+ (at high conc’n: vasoconstriction, BUT at low conc’n in some circumstances: vasodilation)
PgI2 (some prostaglandins cause vasoconstriction & some cause vasodilation).
Describe the interaction b/w the vascular endothelium & the smooth muscle that overlies it.
The endothelium can secrete substances that cause either vasodilation or vasoconstriction of the smooth muscle cells.
What can activate the endothelium to affect the vascular smooth muscle?
A variety of factors, including ACh, platelet aggregation, & sheer stress.
What types of factors can the endothelium release to cause vasodilation?
EDRF (endodermal derived relaxing factor) EDHF NO PgI2 Natriuretic Peptides
What causes the activation of the NO pathway in the endothelium?
Sheer Stress & some chemical substances. Chemical Substances: ACh Endotoxin Cytokines Bradykinin EDRF They all act to increase the intracellular calcium conc'n.
What is the effect of an increase in intracellular calcium in an endothelial cell on the NO pathway?
The increase in intracellular calcium activates the NOS (nitric oxide synthase).
this causes the formation of NO from Arginine.
Once NO is produced in an endothelial cell–>how does it produce vascular smooth muscle relaxation?
The NO diffuses across the endothelial & vascular smooth muscle membranes into the vascular smooth muscle cell.
It activates Guanylyl Cyclase.
the GC enzyme then converts GTP into cGMP which causes the vasorelaxation.
What is the entire NO pathway that causes vasorelaxation of vascular smooth muscle cells?
The endothelium is activated by sheer stress & chemical substances (including ACh, endotoxin cytokines, & bradykinin), which increase the intracellular calcium levels.
The increase in intracellular calcium activates the NOS enzyme, which forms NO from arginine.
The NO diffuses across the membranes into the vascular smooth muscle cells.
The NO activates guanylyl cyclase & forms cGMP from GTP.
The cGMP causes vascular smooth muscle cell relaxation through sequestration of intracellular calcium (less contraction).
What is the overall endothelial response to increased blood flow?
It decrease the velocity of the blood flow in response.
Increased blood flow=increased sheer stress.
Increased sheer stress=increased release of substances like EDRF.
EDRF causes synthesis of NO.
NO activates GC & forms cGMP.
Dilation thru sequestering of intracellular Ca++ & therefore less contraction.
The dilation decreases the velocity of the blood flow.
How does an increase in cGMP in the vascular smooth muscle cells cause vasodilation?
The increased cGMP causes sequestering of intracellular Ca++ & that decreases contractions.
