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RAS
renin aldosterone system
RAS responds to
decreased renal perfusion pressure
Renin secreted by
kidneys (juxtaglomerular cells)
renin converts
angiotensinogen (from liver) to angiotensin I
AC (in lungs) converts angiotensin I →
angiotensin II (AT II)
angiotensin II stimulates
aldosterone → ↑ Na⁺/H₂O reabsorption → ↑ blood volume
angiotensin II Causes
vasoconstriction → ↑ TPR → ↑ BP
Angiotensin II directly enhances
Na⁺ reabsorption in the kidney
aldosterone
steroid hormone released from the adrenal cortex in response to angiotensin II
aldosterone acts on
distal tubule and collecting duct of the nephron
aldosterone promotes
Na⁺ reabsorption and K⁺ secretion
Water follows
sodium → ↑ ECF volume → ↑ blood pressure
Peripheral chemoreceptors
in carotid & aortic bodies
peripheral chemoreceptors detect
↓ O₂ (hypoxia)
↑ CO₂ (hypercapnia)
↓ pH (acidosis)
peripheral chemoreceptors stimulate
sympathetic outflow → vasoconstriction in kidneys, gut, muscle
central chemoreceptors
in medulla
central chemoreceptors respond to
↑ CO₂ and ↓ pH
central chemoreceptors promote
systemic vasoconstriction to prioritize cerebral perfusion
↑ Blood volume stretches atrial baroreceptors →
release of ANP
Atrial natriuretic peptide (ANP)
vasodilation, ↑ renal Na⁺ and water excretion,
↓ ADH and aldosterone secretion
net effect of ANP
↓ blood volume and pressure
Gravity causes blood pooling in the legs →
↓ venous return → ↓ CO → ↓ BP
blood pressure after blood pooling in legs normally corrected by
baroreceptor reflex
baroreceptor reflex
↑ HR, ↑ vasoconstriction
Orthostatic hypotension occurs when
Baroreflex is impaired & ↓ brain perfusion → dizziness, lightheadedness, syncope
In space flight, volume is
lost (no gravity pooling), and orthostatic response is compromised on return to Earth
hyperemia
Increased blood flow to a tissue due to increased metabolic activity or chemical signals
active hyperemia
in response to exercise
reactive hyperemia
following ischemia
Autoregulation of blood flow
local mechanisms maintain constant blood flow despite changes in systemic pressure
autoregulation found in
renal, cerebral, coronary, skeletal muscle, and pulmonary circulations
local vasodilators
CO₂, adenosine, H⁺, lactate, K⁺
effects of local regulation of blood flow
essential during exercise, ischemia, & hypoxia
local vasodilators relax
arterioles → ↑ perfusion to meet tissue demands
myogenic autoregulation
Vessels constrict in response to ↑ pressure; dilate with ↓ pressure
myogenic autoregulation maintains
constant flow despite pressure fluctuations
metabolic autoregulation triggered by
tissue metabolites: ↓ O₂, ↑ CO₂, H⁺, K⁺, adenosine
metabolic autoregulation promotes
vasodilation to increase blood supply during high metabolic activity
systemic regulation of systemic Blood flow maintains
MAP
systemic regulation of systemic Blood flow involves
baroreceptors, RAS, SNS
systemic regulation of systemic Blood flow affects
all organs simultaneously
local control (autoregulation) maintains
tissue perfusion
local control involves
local metabolites and myogenic tone
local control is
organ/tissue specific adjustments
Increased HR and SV→
↑ CO
Vasoconstriction (during exercise) in
gut, kidney, skin (initially)
vasodilation (during exercise) in
skeletal muscle (local metabolites override SNS)
exercise may cause
slight rise in MAP, TPR drops
during exercise, venous return is
enhanced via venoconstriction & muscle pump
Cerebral circulation supplied by
2 carotid & 2 vertebral arteries
cerebral circulation merges into
circle of Willis
cerebral circulation autoregulated via
myogenic, metabolic, & neurogenic
myogenic
pressure/ICP
metabolic
↑ CO₂, ↓ O₂, ↑ H⁺ → vasodilation
neurogenic
minor; protects small vessels from high pressure
blood brain barrier limits
entry of many systemic substances into brain tissue
blood brain barrier prevents
systemic vasoconstrictors/vasodilators from affecting cerebral vessels
blood brain barrier ensures
tight local control of cerebral perfusion
diastolic pressure drops with
decrease in total peripheral resistance