Week 5 Flashcards
Variation in Blood flow requirements
Different blood flow based on metabolic need and support of special functions (kidneys)
Control of blood flow in the arterioles
- Major site of resistance in cardiovascular system (where largest drop in pressure occurs)
- Controlled by hormones and SNS
- Highly muscularly allowing them contract and relax based on signals from local tissues
Feedback loop locally controlling blood flow
- Decrease in O2 delivery or increase in tissue metabolism
- Decrease in tissue O2
- relaxation of arterioles
- increase in tissue blood flow
Active hyperaemia in skeletal muscle
Skeletal muscle can rapidly increase metabolic rate during contraction, leading to rapid increases in blood flow
- increase in hematocrit concentration in blood also increases during contractions (mechanisms not fully understood but could involve changes in the endothelial surface layer (glycocalyx))
Relationship between muscle O2 delivery and muscle O2 consumption rate
- Linear relationship
- Slope is .6 meaning that there is a great increase in delivery relative to O2 consumption (extraction not as efficient)
Misconceptions in active hyperaemia mechanism
Common view:
- capillaries close and do not support blood flow at rest, open following contraction to support more flow
Scientific Observation:
- intravital microscopy has observed most capillaries already support some flow in resting skeletal muscle
New Observation:
- haematocrit within capillaries of resting muscle is much lower than the normal haematocrit in large vessels
Vasodilator Substances
- Released by tissues when they experience low availability of O2 or other nutrients
What substances contribute to blood flow
CO2, H+, lactate, adenosine, adenosine phosphates
- CO2 and H+ play prominent roles in controlling local blood flow in the brain
Why is lactate a good signal for a need in increased blood flow?
- Produced when no oxygen is available to enter citric acid cycle
- Increase in ATP production when increase in energy -> meaning increase lactate production
Why is adenosine a good signal for a need in increased blood flow?
- more ATP broken down with increased activity
- when ATP production meets ATP breakdown, all adenosine is reuptaken into the cell
Communication between capillaries and arterioles
- Endothelial cells can be hyperpolarized in response to local conditions
- cells interconnected by gap junctions - electrical signals can be conducted along vasculature
- endothelial cells in arterioles signal nearby smooth muscle and cause dilation
- Paracrine pathways between successive neighboring endothelial cells may also contribute to communication between capillaries and upstream arterioles
Endothelium derived relaxation factors
- Increase in blood flow causes shear stress
- leads to release of NO (potent vasodilator)
- microvasculature increase flow in larger upstream vessels
Hormones causing vasoconstriction
- Norepinephrine
- Epinephrine
- Angiotensin II
- Antidiuretic Hormone
Hormones causing vasodilation
- Norepinephrine
- Epinephrine
- Bradykinin
- Histamine
Where are the receptors that regulate arterial blood pressure located
Aortic arch and carotid arteries
Cardiovascular control Center
- Located: Brainstem (medulla and pons)
- Receive afferent neural information from sensory receptors and higher centers
- Neurons innervated and control the SNS and PSN
What are the higher centers that send information to the cardiovascular control center
- Temporal
- Orbital
- Cingulate Gyrus
- Motor
- Reticular Substance
- Mesencephalon
SNS anatomy
- Short pre-ganglion axon (Myelinated) going to sympathetic chain ganglion releasing ACh
- Long post-ganglionic axon releasing NE to effector cell
- Some SNS cells pass all the way to the adrenal medulla without synapsing and release ACh at AD
- AD chromaffin cells then releases NE or dopamine into the blood stream
PNS anatomy
- Long lightly myelinated pre-ganglion axon that passes all the way to the target organ without synapsing releasing ACh
- short unmyelinated post-ganglion axon releasing ACh to target organ
SNS and PNS Neurochemistry
PRE-GANGLIONIC NEURONS
- ACh binds to Nicotinic ACh receptors
POST-GANGLIONIC NEURONS
- Parasympathetic system: ACh binds to Muscarinic ACh receptors
- Sympathetic system: NE binds to alpha or beta adrenergic NE receptors
Arterial Baroreceptors
- Sense blood pressure in aorta and carotid sinus
- Baroreceptors are neurons with spray-type nerve endings that are embedded in the artery wall
- Nerve endings depolarize when stretched (Glossopharyngeal in carotid sinus and vagus in aortic)
- Baroreceptor axons project tp the brain and send afferent information to the cardiovascular control centers
Action potential frequency in baroreceptors
- Sensors are always active - baseline frequency
- respond to change (phasic) in BP - most important for short-term regulation
- AP frequency reflects afferent information
- Increase in pressure = increase in AP frequency
- Decrease in pressure = decrease in AP frequency
Efferent pathways in baroreceptors
- SNS neruons innervate the pacemaker and contractile cells in the heart (increase HR and contractility)
- SNS innervates arterioles, which mostly posses alpha adrenergic receptors and constrict in response to SNS
- Arterioles in select organs (heart) posses beta adrenergic and dilate in response to SNS stimulation
- SNS innervates veins causing constriction, increasing venous return
- PNS innervates pacemaker (decrease HR)
Regulated changes in blood pressure
- Locomotion or the stress response activate the SNS and increase BP
- results in a changed setpoint
- increase BP setpoint facilitate increase in systemic BF during periods of high metabolic activity
