L27 Local Control Of Blood Flow Flashcards
Blood flow to an organ will
Increase or decrease depending on organ metabolism
Mechanisms: intrinsic or extrinsic
Intrinsic controllers of blood flow
Independent of neural and hormonal mechanisms
Inherent in tissue
Ex: auto regulation
Extrinsic control of blood flow
Hormonal/neural control
Sympathetic nervous system and various hormones
Blood flow to organs depends on
Interactions btw intrinsic and extrinsic factors
Local mechanisms have two main functions:
Maintain blood flow at constant level under resting conditions
Increase blood flow to a tissue to meet enhanced metabolic needs
Vascular smooth muscle tone
Contractile state of a resistance vessel= vessel tone
Basal tone= state of partial contraction independent of metabolic and neural mechanisms, results from properties of vessel (no external inputs at all)
Vessels can relax or contract further. Wide range of diameters
Resting state= most resistance vessels constricted somewhat more than basal due to sympathetic nerve activity (in vivo) greater than basal tone
Active vasoconstriction
A decrease in vessel diameter due to sympathetic stimulations or constrictor hormones/metabolites
Active vasodilation
An increase in vessel diameter due to dilator nerves, hormones, or local factors
Passive vasoconstriction
Return towards resting state from a dilated state due to the removal of active dilator influences
Passive = withdraw something
Passive vasodilation
Return towards resting state from a constricted state due to the removal of active constrictor influences
Intrinsic mechanisms
Auto regulation
Active(functional) hyperemia
Reactive hyperemia
Auto regulation
Blood flow to a tissue is maintained at a constant level over a physiological range of perfusion pressures
Independent of neural input
Flow maintained by altering the resistance to flow as perfusion pressure changes
Occurs without changes in metabolism
Pressure goes up, blood flow goes up briefly but back to normal by vessel altering its resistance
Metabolic theory of auto regulation
As perfusion pressure increases vasodilator metabolites are washed out of the surrounding interstitial fluid causing passive vasoconstriction and an increase in resistance (conversely vasodilation occurs as metabolites accumulate when pressure falls)
Increase pressure, increase Q, washout metabolic vasodilator, passive vasoconstriction, increase R
Myogenic theory of auto regulation
Increases in P cause increase in wall tension - vascular smooth muscle contracts- R increases
Conversely vasodilation occurs when P falls and wall tension decreases
Stretch sense Ca Channels open = stretch walls= Ca enters cell = contraction = increase R
Metabolic vasodilators
Do not enter the general circ at high enough conc to affect Q in other tissues
Vascular beds may differ in their responsiveness to various vasodilators
K+ CO2 Local hypoxia Lactic acid H+ Phosphate ions (extracellular) Prostaglandins * PGI2 PGE2 Adenosine Adenine nucleotides
Active (functional) hyperemia
Blood adjusted to meet metabolic demands of a tissue
As rate of metabolism increases, blood flow increase, due to increased production of vasodilator metabolites Which cause relaxation of vascular smooth muscle and a decrease in R
Active muscle needs more blood (only affects active bed of any tissue)
Reactive hyperemia
Increase in blood flow to a tissue that occurs in response to transient ischemia
Duration and magnitude of the hyperemia are proportional to time of ischemia
Due to local buildup of vasodilator metabolites during ischemic phase
Ex: weight lifting, cardiac circulation- during systole, heart contracts and obstructs blood flow into coronary artery, majority of perfusion occurs during diastole
Extrinsic mechanisms
SNS
Hormones
Neural control of vascular tone
Sympathetic adrenergic fibers
Control vascular R in most vascular beds
Precapillary resistance vessels are innervated by postganglionic nerves and release norepinephrine
Fibers tonically active in many vascular beds (vasoconstriction)
Contraction mediated via vascular smooth muscle alpah1 adrenergic receptors
SNS vasoconstriction May be attenuated by local vasodilator metabolites or mediators
Withdrawal of sympathetic activity = passive vasodilation
Vasoactive hormones: epinephrine
Contract via alpha1 receptors on vascular smooth muscle of resistance vessels and veins
Relax via beta2 adrenergic receptors on vascular smooth muscle of resistance vessels (mainly skeletal muscle) ( epinephrines primary affinity is for beta2)
Net effect is dependent on epinephrine conc in plasma and relative conc/ affinity of receptors in a tissue
Most tissues = vasoconstriction;
Skeletal muscle = vasodilation due to higher conc beta2 receptors and a greater affinity of beta 2 for epinephrine
Vasoactive hormones: angiotensin II
potent vasoconstrictor acts directly on vascular smooth muscle (AT1 receptors) of resistance vessels
Synthesized when blood pressure is low
Controls release of aldosterone from adrenal cortex
Vasoactive hormones: vasopressin (AKA : AVP, ADH)
Peptide released from posterior pituitary in response to rising plasma osmolarity or low BP
Potent vasoconstrictor acts directly on vascular smooth muscle (V1 receptors) of resistance vessels
Vasoactive substances and vascular tone
Some bind directly to receptors on VSM
Others bind to receptors on endothelial cells and cause release of vasoactive mediators which regulate VSM tone
Ex’s:
NO/vasodilator
PGI2, PGE2 : vasodilator
Endothelin : vasoconstrictor
Histamine: dilates arterioles/ constricts venules
Bradykinin: dilates arterioles/constricts venules
Skeletal muscle circulation
Enormous range of Q in phasic muscle
33ml/min/kg at rest
1000ml/min/kg during exercise
Resistance vessels have high basal tone (myogenic)
Role of skeletal muscle contraction in BP control
Large mass of tissue (40-45% weight)
Major site of resistance vessels
TPR regulated by controlling muscle R
Resistance influence by tonic vasoconstrictor activity, metabolic vasodilators, and regulation by reflex mechanisms (baroreceptors)
Regulations of skeletal muscle Q: neural
Neural control dominates at rest
Tonic SNS vasoconstrictor activity (1Hz)
Alpha1 adrenergic receptor mediated (norepinephrine) TPR and BP can be maintained
Increase SNS activity (4-5Hz) can decrease Q by 70%
Vasodilation at rest is passive due to withdrawal of SNS activity
Regulation of skeletal muscle Q
Metabolism (functional hyperemia)
With increased activity there is an increase in production of vasodilator metabolites
Vasodilator metabolites dominant during exercise ( although SNS activity may also be present)
Main vasodilators: K+, lactate, and adenosine
Coronary circulation control of Q
Major role: local metabolites
Minor role: sympathetic innervation
Local metabolic vasodilators:
Hypoxia (decrease PO2)
Vasodilators (adenosine, NO, CO2, H+, prostaglandins)
Increase contractility = increase O2 demand/use= local hypoxia = vasodilation = increase Q (active hyperemia)
Auto regulation range: 50-60 mmHg to 150-160 mmHg
Coronary circulation
Role of mechanical compression during systole I
Coronary vessels subject to compressive forces within wall of myocardium ( greater than in diastole)
Only about 20% total coronary flow occurs during systole
Compressive forces less marked in right ventricle due to smaller muscle mass and lower ventricular pressure development
Coronary circulation
Reactive hyperemia
Brief occlusion of coronary vessel is followed by transient increase in coronary Q
Occlusion results in accumulation of vasodilator metabolites in interstitium
Magnitude / duration of extra flow dependent on duration of occlusion
Coronary circulation
Neural considerations
Sympathetic stimulation:
Coronary arteries and arterioles
Norepinephrine- alpha1 - constrictor
Epinephrine - beta2 - vasodilation (minor one ventricles)
Heart
Beta1 - increase HR, contractility
Local metabolism- vasodilators- increase Q
In active heart, metabolic vasodilators overcome neural vasoconstriction
Net effect: increase Q to myocardium when SNS active
