The Vasculature Flashcards
Definition of atherosclerosis
Build up of cholesterol rich plaques, causes stenosis of artery
Made up of an atherosclerotic lesion and fibrous cap
Definition of acute coronary syndrome
Symptoms associated with decreased blood flow in coronary arteries
As a result, part of heart muscle can’t function/dies
Definition of tunica adventitia
Tough outermost layer of collagen fibres, supportive element (ext elastic lamina)
Definition of tunica media
Mainly made up of smooth muscle and elastic fibres
Thickest layer
Definition of tunica intima
Made up of 1 layer of endothelial cells, supported by int elastic lamina
Definition of oxidative stress
Overproduction of reactive oxygen species
Definition of resistance arteries
Small diameter blood vessel in microcirculation that contributes to creation of resistance to flow
Definition of autoregulation
Blood flow in vascular beds remain fairly constant over a wide range of pressures
Due to myogenic response and effects of flow on local conc of metabolites
Definition of hyperaemia
Increased volume of blood supplying the vessels
Definition of reactive hyperaemia
If local blood flow cut off, metabolites accumulate => VD
When blood flow resumed, transiently enhanced until metabolites wash out
Definition of pericytes
Smooth muscle found in CNS capillaries
Definition of orthostasis
Decreased BP when you stand up
What are the functions of the 3 circulatory systems
- arterial
- venous
- micro
Arterial
-regulates blood distribution as high pressures can damage
Venous
- 60-70% of all blood here
- VC redistributes blood to maintain CO, BP
Micro
-gas, nutrient, waste product exchange
Describe the composition of arteries
- tunica ext
- tunica med
- tunica int
Tunica ext
-collagen, vessels, fibroblasts, sympathetics
tunica med
- surrounded by ext/int elastic lamina
- SM, control diameter
tunica int
-endothelium (regulate VD, VC, angiogenesis)
Describe the importance of vascular tone
-2 reasons
Maintain flow to organs via VC, VD
Control BP via CO, TPR
Describe the mechanism for SM contraction and relaxation
-what inhibits and activates MP
Myosin + Calmodulin + Ca2+ = (MLCK)=> MyosinPi
MyosinPi =(MP)=> Myosin + Calmodulin + Ca2+
MP
-activated by NO via cGMP => decreases Ca sensitivity
-inhibited by rho kinase => increases Ca sensitivity
Describe how vascular smooth contraction is stimulated by a1 (NA, angiotensin II)
Rho kinase activated => Ca sensitization
Phospholipase C splits PIP2 => IP3
IP3 acts on SR => increase [Ca]
IP3 + DAG activates receptor gated Na channels => increase [Na]
Stretch activated Na activate => increase [Na]
Increased [Na] => depolarization => opening of voltage gated Ca channels => increases [Ca]
How is NO released from the endothelial cells
VD substance binds to receptor => increased [Ca] => activates eNO synthase
Sheer flow phosphorylates Akt =>activates eNOs
Arginine =(eNOs)=> NO
NO diffuses across to smooth muscle
How does NO cause smooth muscle relaxation
NO activates GC
GC converts GTP => cGMP => Ca desensitization
cGMP => Ca uptake into SERCA and Ca removal via CaATPase
cGMP => K removal via K channels => hyperpolarisation
=> voltage gated Ca close, inhibit Ca uptake
PDE converts cGMP => GMP
How does the endothelium promote VD when the NO system is not working sufficiently
-2 mechanisms
VD substances => VGKC open => K out => hyperpolarisation spreads
EETs released by endothelium => activate SM K channels
Describe how VD substances can cause VD in SM
Activation of B2, PGI2, ADO receptors of SM => AC => increased cAMP => PKA => VD
How does the SNS regulate vascular tone
- what is the function
- which regions are affected
Redistributes flow by increasing TPR
Widespread constriction in
- splanchnic
- renal
- cutaneous
- muscle
How does the PNS regulate vascular tone
- what is the function
- what regions are affected
V discrete effects, no change in TPR
Regulates organ flow
- salivary
- GI
- penile
- pancreas
How do these hormones affect vascular tone
- Adrenaline
- AngII, ADH
Adrenaline
-VD => increase flow to muscles
AngII, ADH
-VC => increase BP
How do these local metabolites affect vascular tone
- Prostaglandins (endothelium released)
- Seretonin
-ADO
- Endothelin (endothelium released)
- EET (endothelium released
Prostaglandins
-VD, oppose haemostasis
Seretonin
-VC, promote haemostasis
ADO
-VD, muscle metabolite
Endothelin
-VC
EET
-VD
What molecules promote NO release from the endothelium
-what are their effects
Bradykinin ATP Histamine Increased CO2 Ach Blood flow
VD
Describe the myogenic response
- what arterioles does this occur in
- what is its function
Sudden increase in P => increased diameter => increased F => SAC activated, depolarize, contract => VC
Decreased P => decreased F => slow VD
MAINTAIN CONSTANT LEVEL OF FLOW
Larger arterioles
Describe the metabolic regulatory response
- what arterioles does this occur in
- what is its function
Metabolites => VD => increased F
Metabolites washed away => decreased VD => increased R => decreased F
LIMITED TO ACTIVE MUSCLE
FLOW PROPORTIONAL TO METABOLIC RATE
Smaller arterioles
Describe reactive hyperemia
-what types of exercise result in this
Local flow cut off => VD due to accumulation of metabolites => increased F until metabolites washed away
ISOMETRICS
Describe the CO distribution at rest
- what organs get the most
- what are the properties of flow here
Kidney, brain, heart
- v low R
- vulnerable to changes in F and P
What are the anatomical adaptations of coronary flow
Coronary collaterals
1 cap/myocytes
What are the physiological adaptations of coronary flow
Myogenic, metabolic response
High O2 extraction, only increased via increased F
What are the drawbacks of coronary flow
Flow in L coronary occluded in LV systole => endocardium perfused in diastole
If diastole shortens => reduced F
Describe how the coronary flow reserve normally operates
What happens when the VD mechanism does not function
F = ∆P/R
Normally as R increases => ∆P increases => F maintained
As R increases => ∆P does not increase enough => F falls
What are the anatomical adaptations of cerebral flow
Circle of Willis anastomosis
High capillary density
BBB controls substance mv
What are the physiological adaptations of cerebral flow
Metabolic hyperemia
Weak ANS control
Describe how VC is stimulated in the cerebral circulation
Neuronal glutamate release => Astrocytes release 20HETE
Describe how VD is stimulated in the cerebral circulation
Neuronal NO, PGE2
Neuronal glutamate => Astrocytes release K, EET, PGE2
Hyperpolarization spread via gap junctions
Describe the typical composition of veins
Same as arteries but
- sparse SM
- collapsible
How does venous blood return to the heart
Decreased R than arterial system
Skeletal muscle pump of deep veins w valves
Resp pump, inspiration reduced thorax P => decreased vena cava P => increased P difference => draws blood in
Describe the composition of capillaries
-2 structures
Basal lamina
-fibrous support for endothelium
Endothelium
-material exchange
