Describe the autoregulation of renal blood flow.

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College Answer

To achieve a pass in this question, candidates needed to briefly define autoregulation and
state the range of Mean Arterial Pressure over which this occurs, and why it occurs, then
provide a more detailed discussion about the mechanisms thought to be responsible for
this.
The main site of autoregulation in the kidney is the afferent arteriole. There are two main
factors that affect vascular tone in the afferent arteriole, these are stretch-activated
constriction of vessels (myogenic mechanism) and tubulo-glomerular feedback (TGF).
Both of the above mechanisms are important to maintenance of near-constant blood flow.
Stretch results in membrane depolarisation, increased intra-cellular concentrations of
calcium ions, and ultimately, vasoconstriction.
In tubulo-glomerular feedback, complex signals pass from the macula densa to the
afferent arteriole, regulating its tone. The fundamental theme of TGF is that increased
delivery of fluid and/or NaCl to the distal tubule causes vasoconstriction, thus limiting the
flow (negative feedback).
The major weakness in answers was again the failure to include sufficient information to
achieve a pass mark

Discussion

  • Renal blood flow
    • Total blood flow: 20-25% of cardiac output, or 1000ml/min, or 400ml/100g/min
      • 95% goes to the cortex, 5% goes to the medulla
      • Medullary blood flow must remain low to maintain the urea concentration gradient, to facilitate the concentration of urine
    • Total renal blood is high for reasons of filtration rather than metabolism
    • Total renal oxygen extraction is low (10-15%)
    • Renal oxygen extraction remains stable as renal blood flow changes, because renal metabolic rate depends on glomerular filtration rate and tubular sodium delivery
  • Autoregulation of blood flow:
    • This is a property of regional circulatory systems which allows them to maintain stable blood flow over a range of changing pressure conditions
  • Autoregulation of renal blood flow
    • Renal blood flow remains constant over a MAP range of 75-160 mmHg
    • This regulation is produced by:
      • Myogenic response (50% of the total autoregulatory response)
      • Tubuloglomerular feedback (35%)
      • Other mechanisms involving angiotensin-II and NO (<15%)
    • Intrinsic myogenic mechanisms:
      • Vasoconstriction in response to wall stretch
      • This is a stereotyped vascular smooth muscle response, not unique to the kidney
    • Tubuloglomerular feedback
      • This is a negative feedback loop which decreases renal blood in response to increased sodium delivery to the tubule
      • The mechanism is mediated by ATP and adenosine secreted by macula densa cells, which cause afferent arterolar vasoconstriction
  • Sympathetic regulation of renal blood flow
    • Sympathetic tone regulates the range fo renal blood flow autoregulation
    • Autoregulation typically maintains stable renal blood flow over a wide range of systemic sympathetic conditions
    • Massive sympathetic stimulus (eg. shock) overrides autoregulation and markedly decreases renal blood flow
    • Glomerula filtration rate is less affected (out of porportion to blood flow) because the efferent arterioles vasoconstrict more than the afferent in response to a sympathetic stimulus.

References

Just, Armin. "Mechanisms of renal blood flow autoregulation: dynamics and contributions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292.1 (2007): R1-R17.

Stein, Jay H. "Regulation of the renal circulation." Kidney international 38.4 (1990): 571-576.

Bertram, John F. "Structure of the renal circulation." Advances in Organ Biology Volume 9, 2000, Pages 1-16 (2000)

Kriz, Wilhelm, and Brigitte Kaissling. "Structural organization of the mammalian kidney." The kidney: physiology and pathophysiology 3 (1992): 587-654.

Braam B., Yip S., Cupples W.A. (2014) Anatomy, Physiology, and Pathophysiology of Renal Circulation. In: Lanzer P. (eds) PanVascular Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-37393-0_146-1