lec 8 - aorta to arterioles

arteries structure

high elastic tissue for elastic recoil

arterioles structure

high smooth muscle - contraction and relaxation

arterioles vs arteries structure

proportion of smooth muscle and elastic tissue is different - structure related to function 

function of aorta (and other large elastic arteries)

distribute blood

pressure reservoir - reduce fluctuations in pressure and flow - maintain flow throughout the cardiac cycle

pressure reservoir

systole - stretching stores potential energy

diastole - recoil to release stored energy

recoil during diastole causes blood flow away from the heart as the aortic valve shuts

maintains arterial flow throughout the cardiac cycle

ageing and cardiovascular disease

compliance is inveresley proportional to stiffness 

arteries have high compliane 

when you age get decreased compliance and increased stiffness = dysregulated blood flow 

function of arterioles 

smooth muscle cells wrap around the vessel 

contraction squeezes the lumen to reduce diameter = vasoconstriction 

main determinant of resistance (local and total peripheral resistance) 

important in controlling regional blood flow 

arterial blood pressure

minimum pressure just before ventricle contraction = diastolic pressure (DP)

maximum arterial pressure during peak ventricular ejection = systolic pressure (SP)

MAP = DP + 1/3 x PP

normal is 120/80

dicrotic notch

aortic valve shuts

transient increase in pressure 

determinants of arterial blood pressure

MAP = Q x TPR

Q in this case is CO

TPR is sum of global resistance (from all systemic vascular beds) 

arterial pressure depends on both so can be mantained by alterations to either 

• decreased MAP → vasoconstriction = increased TPR = increased MAP

• decreased map → increased HR → increased Q → increased MAP

MAP is a critical homeostatic variable 

blood flow distribution

regionally blood flow can be dynamically regulated to match demand

changes in local resistance (through arterioles constricting or dilating)

different reponses in vascular beds - cause MAP to remain stable

blood flow redistribution - how

altered metabolic demands

no change in pressure gradient → differential changes in regional resistance → same total volume is redistributed - regional changes to flow 

different responses in vascular beds - MAP remains stable 

what mechanisms to control vascular diameter

complex control systems

neural, hormonal and local controls 

flexibility

neural control mechanisms - extrinsic control symoathetic

sympathetic nervous system → noradrenaline → binds to alpha1-adrenergic receptors → vasoconstriction 

types of receptors in different tissues

in brain: low numbers of alpha1 adrenergic receptors = limited vasoconstriction - important because brain needs constant flow 

skin and GI: high numbers of alpha1-adrenergic receptors = vasoconstriction - important because flow needs to be flexible 

non cholingeric/non-adrenergic - extrinsic control

postganglionic autonomic nerves → nitric oxide → relaxes smooth muscle cells → vasodilation

specalised innervation system - not widespread 

GI system 

reproductive (penis)

hormonals and effects dilation vs constriction

ciculating hormones can alter vascular diameter 

constriction (aldrenaline, angiotensin II, vasopressin)

dilation (adrenaline, atrial natriuretic peptide)

blood vessles have alpha1 and beta2 adrenergic receptors 

a1:b2 ratio

tissue/organ specific which related to function

skin - predominant alpha1 - vasoconstriction

skeletal muscle - predominantly b2 - vasodilation

long term control of CO - hormonal

hormones that play a role in long term regulation of MAP are also vasoactive

increase blood volume:

ADH - increases water reabsorption

angiotensin II - stimulates Na+ (and therefore H2O) reabsorption

= vasoconstriction

decreased blood volume:

atrial natriuretic peptide - decreases water reabsorption = vasodilation

local control mechanisms - intrinsic control

local factors can alter vascular diameter

no nerves or hormones involved 

autoregulation 

active hyperemia (aka metabolic autoregulation) = dilation 

flow autoregulation (aka myogenic autoregulation), reactive hyperemia = constriction/dilation

active hyperemia

blood flow changes to match changes in local metabolism

tissue specific responses

based on metabolism - highly developed in skeletal and cardiac tissue (with high metabolic demands)

flow autoregulation

control of blood flow to maintain flow with changes in perfusion pressure

no changes in local metabolism

myogenic = from muscles 

autoregulation maintains a steady flow - similar over a wide range of pressures 

outside autoregulation range - flow not constant as limits of constriction/dilation reached 

increased pressure stretxhed smooth muscle cells and causes vasoconstriction 

in contrast: