Autoregulation - Cardiovascular

Introduction
- Autoregulation is a mechanism that ensures constant blood flow to organs, despite changing resistance (perfusion pressures) in the blood vessels
  - 2 hypotheses explain autoregulation
    
    myogenic hypothesis
    
    metabolic hypothesis
  - recall that blood flow (Q) = (change in pressure [P])/resistance (R)

                        Hypotheses of Autoregulation
                    
                        Myogenic hypothesis 
                    
                        when the vascular smooth muscle is stretched (like when arterial pressure is increased), the smooth muscle contracts (increases resistance)
                    
                        when there is an increase in blood pressure, the myogenic reflex causes smooth muscle contraction in order to maintain flow
                    
                        Metabolic hypothesis 
                    
                        O2 delivery to a tissue is matched to O2 consumption of that tissue
                    
                        this is accomplished by changing the resistance (and blood flow) of the arterioles
                    
                        metabolic activity causes tissues to produce metabolites, including vasodilators
                    
                        CO2, H+, K+, lactate, and adenosine
                    
                        ↑ metabolic demand → ↑ O2 demand → vasodilation → ↓ resistance
                    
                        this results in ↑ blood flow
                    
                        Autoregulation of Organs
OrganFactors Determining Autoregulation
HeartLocal metabolitespO2, adenosine, pCO2, and NO
BrainLocal metabolitespCO2 andpH
KidneysMyogenic hypothesistubuloglomerular feedback
LungsLocal metabolitespO2→ vasoconstriction
Skeletal musclesLocal metaboliteslactate,K+, and adenosine
SkinSympathetic innervation

Organ-Specific Autoregulation
- Heart
  - most sensitive to
    
    pO₂, adenosine, pCO₂, and NO
    
    adenosine results in coronary vasodilation
  - ↑ myocardial contractility → ↑ O₂ demand and consumption → vasodilation → ↑ blood flow
- Brain
  - most sensitive to
    
    pCO₂ and pH
  - ↑ pCO₂ → ↓ pH → vasodilation→ ↑ blood flow to remove excess CO₂
- Kidneys
  - myogenic hypothesis
  - tubuloglomerular feedback
    
    ↑ renal arteriole pressure → ↑ blood flow
    
    ↑ glomerular filtration rate (GFR)
    
    ↑ GFR increases delivery of solute and water to juxtaglomerular apparatus (JGA)
    
    JGA secretes vasoactive substance
    
    constriction of afferent arterioles
    
    returns renal blood flow and GFR back to normal
- Lungs
  - most sensitive to
    
    low pO₂, which causes vasoconstriction NOT vasodilation
    
    the only organ in which low pO₂ causes vasoconstriction
    
    causes only well-ventilated areas to be perfused to maximize areas of gas exchange
- Skeletal muscles
  - most sensitive to
    
    vasoactive metabolites during exercise (e.g., lactate, K⁺, and adenosine)
    
    sympathetic innervation at rest
    
    recall that α1 receptors cause vasoconstrict and β2 receptors cause vasodilation
- Skin
  - most sensitive to sympathetic innervation
    
    ↓ body temperature → α1 receptors vasoconstrict
    
    ↓ blood flow → retention of heat
    
    ↑ body temperature → inhibition of cutaneous vasoconstriction
    
    ↑ blood flow from warm core to cutaneous vessels → dissipation of heat
  - plays a major role in the regulation of body temperature

Autoregulation of Organs
Organ	Factors Determining Autoregulation
Heart	Local metabolites pO₂, adenosine, pCO₂, and NO
Brain	Local metabolites _{pCO₂ andpH}
Kidneys	Myogenic hypothesis tubuloglomerular feedback
Lungs	Local metabolites pO₂→ vasoconstriction
Skeletal muscles	Local metabolites lactate,K⁺, and adenosine
Skin	Sympathetic innervation

Action	Numeric Key	Letter Key	Function Key
Show Bullets		S	Enter (frontside only)
20%	1	N
40%	2	H
60%	3	F	Enter (backside only)
80%	4	E
100%	5	M
Toss	0	T