Lecture 6: Regulation of Blood Pressure by Other Systems & Exercise

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Last updated 3:41 PM on 6/5/26
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59 Terms

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RAS

renin aldosterone system

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RAS responds to

decreased renal perfusion pressure

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Renin secreted by

kidneys (juxtaglomerular cells)

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renin converts

angiotensinogen (from liver) to angiotensin I

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AC (in lungs) converts angiotensin I →

angiotensin II (AT II)

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angiotensin II stimulates

aldosterone → ↑ Na⁺/H₂O reabsorption → ↑ blood volume

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angiotensin II Causes

vasoconstriction → ↑ TPR → ↑ BP

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Angiotensin II directly enhances

Na⁺ reabsorption in the kidney

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aldosterone

steroid hormone released from the adrenal cortex in response to angiotensin II

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aldosterone acts on

distal tubule and collecting duct of the nephron

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aldosterone promotes

Na⁺ reabsorption and K⁺ secretion

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Water follows

sodium → ↑ ECF volume → ↑ blood pressure

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Peripheral chemoreceptors

in carotid & aortic bodies

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peripheral chemoreceptors detect

↓ O₂ (hypoxia)

↑ CO₂ (hypercapnia)

↓ pH (acidosis)

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peripheral chemoreceptors stimulate

sympathetic outflow → vasoconstriction in kidneys, gut, muscle

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central chemoreceptors

in medulla

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central chemoreceptors respond to

↑ CO₂ and ↓ pH

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central chemoreceptors promote

systemic vasoconstriction to prioritize cerebral perfusion

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↑ Blood volume stretches atrial baroreceptors →

release of ANP

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Atrial natriuretic peptide (ANP)

vasodilation, ↑ renal Na⁺ and water excretion,

↓ ADH and aldosterone secretion

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net effect of ANP

↓ blood volume and pressure

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Gravity causes blood pooling in the legs →

↓ venous return → ↓ CO → ↓ BP

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blood pressure after blood pooling in legs normally corrected by

baroreceptor reflex

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baroreceptor reflex

↑ HR, ↑ vasoconstriction

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Orthostatic hypotension occurs when

Baroreflex is impaired & ↓ brain perfusion → dizziness, lightheadedness, syncope

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In space flight, volume is

lost (no gravity pooling), and orthostatic response is compromised on return to Earth

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hyperemia

Increased blood flow to a tissue due to increased metabolic activity or chemical signals

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active hyperemia

in response to exercise

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reactive hyperemia

following ischemia

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Autoregulation of blood flow

local mechanisms maintain constant blood flow despite changes in systemic pressure

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autoregulation found in

renal, cerebral, coronary, skeletal muscle, and pulmonary circulations

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local vasodilators

CO₂, adenosine, H⁺, lactate, K⁺

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effects of local regulation of blood flow

essential during exercise, ischemia, & hypoxia

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local vasodilators relax

arterioles → ↑ perfusion to meet tissue demands

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myogenic autoregulation

Vessels constrict in response to ↑ pressure; dilate with ↓ pressure

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myogenic autoregulation maintains

constant flow despite pressure fluctuations

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metabolic autoregulation triggered by

tissue metabolites: ↓ O₂, ↑ CO₂, H⁺, K⁺, adenosine

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metabolic autoregulation promotes

vasodilation to increase blood supply during high metabolic activity

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systemic regulation of systemic Blood flow maintains

MAP

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systemic regulation of systemic Blood flow involves

baroreceptors, RAS, SNS

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systemic regulation of systemic Blood flow affects

all organs simultaneously

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local control (autoregulation) maintains

tissue perfusion

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local control involves

local metabolites and myogenic tone

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local control is

organ/tissue specific adjustments

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Increased HR and SV→

↑ CO

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Vasoconstriction (during exercise) in

gut, kidney, skin (initially)

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vasodilation (during exercise) in

skeletal muscle (local metabolites override SNS)

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exercise may cause

slight rise in MAP, TPR drops

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during exercise, venous return is

enhanced via venoconstriction & muscle pump

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Cerebral circulation supplied by

2 carotid & 2 vertebral arteries

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cerebral circulation merges into

circle of Willis

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cerebral circulation autoregulated via

myogenic, metabolic, & neurogenic

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myogenic

pressure/ICP

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metabolic

↑ CO₂, ↓ O₂, ↑ H⁺ → vasodilation

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neurogenic

minor; protects small vessels from high pressure

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blood brain barrier limits

entry of many systemic substances into brain tissue

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blood brain barrier prevents

systemic vasoconstrictors/vasodilators from affecting cerebral vessels

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blood brain barrier ensures

tight local control of cerebral perfusion

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diastolic pressure drops with

decrease in total peripheral resistance