AfraTafreeh.com
Last edited: 3/7/2022
AUTOREGULATION
Renal | Autoregulation (updated) Medical Editor: Gerard Jude Loyola
OUTLINE
I) RENAL AUTOREGULATION IV) APPENDIX
II) INTRINSIC MECHANISMS V) REVIEW QUESTIONS
III) EXTRINSIC MECHANISMS VI) REFERENCES
I) RENAL AUTOREGULATION
Ability of the kidney to modify the blood flow and urine output
How?
o Intrinsic mechanisms: o Extrinsic mechanisms:
Myogenic mechanism Sympathetic nervous system
Tubuloglomerular feedback Renin-angiotensin-aldosterone-ADH system
(RAAS)
II) INTRINSIC MECHANISMS
(A) MYOGENIC MECHANISM
Myogenic = muscle of afferent arteriole
Blood pressure is a surrogate of the glomerular hydrostatic pressure
o Glomerular hydrostatic pressure (GHP): pressure inside the capillaries exerted to push substances out of the capillaries and
into the Bowman’s capsule
(1) ↑BP (2) ↓BP
Figure 1. Myogenic mechanism during increased blood
pressure. AA – afferent arteriole, EA – efferent arteriole, BC – Figure 2. Myogenic mechanism during decreased blood
Bowman’s capsule, PCT – proximal convoluted tubule pressure.
↑BP → ↑GHP → ↑GFR ↓BP → ↓GHP → ↓GFR
o Higher glomerular filtration rate (GFR), more urine o ↓BP = ↓urine = can cause kidney injury
Kidneys modulate the GFR so that it is not too excessive o How does the kidney prevent it?
making too much urine, or the blood pressure does not
(i) Mechanism:
remain too high causing injury on the glomerular
capillaries ↓BP = ↓blood to the AA = ↓stretch on the AA
↓stretch → ↓Na+ enter in the smooth muscle cell → less
(i) Mechanism: positive charge → ↓Ca2+ released by the sarcoplasmic
Blood flows through the AA then to the EA reticulum → ↓contraction = relaxation
↑BP = more blood to the AA
Summary:
↑BP = ↑GFR
o Counteracted by vasoconstriction of AA → ↓GFR
o Na channels in the smooth muscle is sensitive to ↓BP = ↓GFR
stretch o Counteracted by vasodilation of AA → ↑GFR
AA vasoconstricts → ↓glomerular blood flow (GBF) →
↓filtered plasma and other substance (↓GFR)
AUTOREGULATION RENAL PHYSIOLOGY: Note #1. 1 of 5
AfraTafreeh.com
, AfraTafreeh.com
(B) TUBULOGLOMERULAR FEEDBACK
This mechanism is sensitive to NaCl
o NaCl gets reabsorbed in the proximal convoluted tubule (PCT)
(1) ↑BP (2) ↓BP
Figure 3. Tubuloglomerular feedback mechanism on high blood Figure 4. Tuberoglomerular feedback mechanism on low blood
pressures. MDC – Macula densa cells, DCT – distal convoluted pressures.
tubule, LH – loop of Henley, JG cells – juxtoglomerular cells
↓BP = ↓GFR = ↓NaCl excretion into the kidney tubules
When macula densa cells detect ↓NaCl in DCT, they
↑BP = ↑GFR = ↑NaCl excretion into the kidney tubules
AfraTafreeh.com release PGI2 and nitric oxide (NO)
When NaCl transporters in the PCT are saturated, NaCl PGI2 and NO function to:
can escape and move to the LH and then to the DCT o (1) vasodilate the AA → ↑GBF → ↑GFR → ↑NaCl
where macula densa cells are found filtered
o Special NaCl sensors
o Release adenosine when it detects ↑NaCl
Adenosine functions to:
o (1) vasoconstrict AA → ↓GBF → ↓GFR → ↓NaCl Summary:
being filtered ↑BP = ↑GFR = ↑NaCl filtered
o (2) inhibit juxtaglomerular (JG) cells → ↓renin → o ↑NaCl detected by MD cells → release adenosine
→ vasoconstricts AA and inhibits JG cells to
↓blood pressure
release renin
Remember: ↓BP = ↓GFR = ↓NaCl filtered
Renin functions to increase blood pressure through a o ↓NaCl detected by MD cells → release PGI2 and NO
complicated process. → vasodilates AA and stimulates JG cells to
release renin
2 of 5 RENAL PHYSIOLOGY: Note #7. AUTOREGULATION
Last edited: 3/7/2022
AUTOREGULATION
Renal | Autoregulation (updated) Medical Editor: Gerard Jude Loyola
OUTLINE
I) RENAL AUTOREGULATION IV) APPENDIX
II) INTRINSIC MECHANISMS V) REVIEW QUESTIONS
III) EXTRINSIC MECHANISMS VI) REFERENCES
I) RENAL AUTOREGULATION
Ability of the kidney to modify the blood flow and urine output
How?
o Intrinsic mechanisms: o Extrinsic mechanisms:
Myogenic mechanism Sympathetic nervous system
Tubuloglomerular feedback Renin-angiotensin-aldosterone-ADH system
(RAAS)
II) INTRINSIC MECHANISMS
(A) MYOGENIC MECHANISM
Myogenic = muscle of afferent arteriole
Blood pressure is a surrogate of the glomerular hydrostatic pressure
o Glomerular hydrostatic pressure (GHP): pressure inside the capillaries exerted to push substances out of the capillaries and
into the Bowman’s capsule
(1) ↑BP (2) ↓BP
Figure 1. Myogenic mechanism during increased blood
pressure. AA – afferent arteriole, EA – efferent arteriole, BC – Figure 2. Myogenic mechanism during decreased blood
Bowman’s capsule, PCT – proximal convoluted tubule pressure.
↑BP → ↑GHP → ↑GFR ↓BP → ↓GHP → ↓GFR
o Higher glomerular filtration rate (GFR), more urine o ↓BP = ↓urine = can cause kidney injury
Kidneys modulate the GFR so that it is not too excessive o How does the kidney prevent it?
making too much urine, or the blood pressure does not
(i) Mechanism:
remain too high causing injury on the glomerular
capillaries ↓BP = ↓blood to the AA = ↓stretch on the AA
↓stretch → ↓Na+ enter in the smooth muscle cell → less
(i) Mechanism: positive charge → ↓Ca2+ released by the sarcoplasmic
Blood flows through the AA then to the EA reticulum → ↓contraction = relaxation
↑BP = more blood to the AA
Summary:
↑BP = ↑GFR
o Counteracted by vasoconstriction of AA → ↓GFR
o Na channels in the smooth muscle is sensitive to ↓BP = ↓GFR
stretch o Counteracted by vasodilation of AA → ↑GFR
AA vasoconstricts → ↓glomerular blood flow (GBF) →
↓filtered plasma and other substance (↓GFR)
AUTOREGULATION RENAL PHYSIOLOGY: Note #1. 1 of 5
AfraTafreeh.com
, AfraTafreeh.com
(B) TUBULOGLOMERULAR FEEDBACK
This mechanism is sensitive to NaCl
o NaCl gets reabsorbed in the proximal convoluted tubule (PCT)
(1) ↑BP (2) ↓BP
Figure 3. Tubuloglomerular feedback mechanism on high blood Figure 4. Tuberoglomerular feedback mechanism on low blood
pressures. MDC – Macula densa cells, DCT – distal convoluted pressures.
tubule, LH – loop of Henley, JG cells – juxtoglomerular cells
↓BP = ↓GFR = ↓NaCl excretion into the kidney tubules
When macula densa cells detect ↓NaCl in DCT, they
↑BP = ↑GFR = ↑NaCl excretion into the kidney tubules
AfraTafreeh.com release PGI2 and nitric oxide (NO)
When NaCl transporters in the PCT are saturated, NaCl PGI2 and NO function to:
can escape and move to the LH and then to the DCT o (1) vasodilate the AA → ↑GBF → ↑GFR → ↑NaCl
where macula densa cells are found filtered
o Special NaCl sensors
o Release adenosine when it detects ↑NaCl
Adenosine functions to:
o (1) vasoconstrict AA → ↓GBF → ↓GFR → ↓NaCl Summary:
being filtered ↑BP = ↑GFR = ↑NaCl filtered
o (2) inhibit juxtaglomerular (JG) cells → ↓renin → o ↑NaCl detected by MD cells → release adenosine
→ vasoconstricts AA and inhibits JG cells to
↓blood pressure
release renin
Remember: ↓BP = ↓GFR = ↓NaCl filtered
Renin functions to increase blood pressure through a o ↓NaCl detected by MD cells → release PGI2 and NO
complicated process. → vasodilates AA and stimulates JG cells to
release renin
2 of 5 RENAL PHYSIOLOGY: Note #7. AUTOREGULATION
