Chemoreceptors

Baroreceptors

• Detect stretch related to pressure and volume

• Helps maintain pressure and volume hemostasis

Chemoreceptors

Detect changes in O2, CO2, and pH

• allow the respiratory and cardiovascular control centers o recognize that the chemical environment is changing and initiate a homestatic response

Peripheral chemoreceptors

They monitor decrease in O2, increased in CO2 and decrease in pH (not as much)

Peripheral chemoreceptors - carotid bodies

• signal travels through CN IX (glossopharyngeal)

• near carotid bifurcation

Peripheral chemoreceptors - aortic bodies

• signal travels through CN X (vagus nerve)

• near aortic arch

Why does the body monitor O2, CO2, and pH

the body needs a way to detect when:

• O2 avalability is becoming inadequate

• CO2 is accumulating

• pH is falling

Stimulus of chemocreceptors

Decrease in O2, increase in CO2 or decrease in pH

Receptor

Peripheral chemoreceptors

Afferent pathway

Carotid body → CN IX

Arotic body → CN X

Integration

Brainstem respiratory center

Efferent output

Motor signals to the respiratory muscles

Effector

Diagphram and respiratory muscles

Response

Increase rate and or depth of ventilation

Central chemoreceptors

• location- medulla of brainstem

• More sensitive to CO2

Two ways to protect blood pressure and perfusion

• neural reflexes

• RAAS system

Neural reflexes

Rapid response

• barorreceptors detect changes in pressure/ stretch

• Chemoreceptors detect changes in O2, CO2, and [pH

• Signals are integrated in the brainstem

• Autonomic response occur within seconds

RAAS

A hormonal system that helps defend blood pressure, circulating volume, and tissue perfusion

• kidneys play central roles

Why do we need RAAS

• blood pressure needs to be restored

• Volume needs to be conserved

• RAAS helps accomplish both

what is the overall goal of increasing vascular resistance and circulating volume

restore blood pressure and maintain tissue perfusion

How does the kidney know there is a problem

Afferent arterioles → glomerulus → efferent arterioles → juxtaglomerular apparatus (JGA) — helps kidney recognize when renal perfusion or filtration may be inadequate

3 signals trigger renin release

1. Decreased renal perfusion pressure

2. Decreased NaCl delivery to the macula densa

3. Increased sympathetic stimulation

Renin

enzyme released by the juxtagolermular cells of the kidney

Decrease renal perfusion pressure

Less stretch of JG cells in the afferent arterioles → renin released

Decreased NaCl delivery to the macula densa

Suggests decreased tubular flow/ filtration → signals JG cells → renin release

Increased sympathetic stimulation

Beta receptors on JG cells → renin release

Angiotensins I to Angiotensin II

Angiotensin I is converted to angiotensin II by an enzyme by ACE

ACE

Present on vascular endothelial cells and is particularly abundant in the pulmonary circulation

Angiotensin II

Major effector of RAAS

What does angiotensin II promotes

Promotes:

• constriction blood vessel → raise SVR

• Retain Na → retain volume

• Retain water → retain volume

• Increase water intake → add volume

Angiotensin II: vasoconstriction

Binds receptors on vascular smooth muscle causing arteriol vasoconstriction → increases SVR → increase in blood pressure

Angiotensin II: kidneys

constricts efferent arteriole

what effect does constricting efferent arterioles have

• resistance to blood leaving the glomerulus increase

• helps miantian glomerulus pressure

• helps preserve filtration when renal perfusion falls

why does the RAAS system happen

Because the body is trying to maintain pressure, conserve volume, and preserve tissue perfusion