Cerebral autoregulation maintains relatively constant cerebral blood flow (CBF) over a range of mean arterial pressures. The primary mechanism of myogenic autoregulation in cerebral vessels involves:
- A Endothelial NO release increasing when wall tension rises, causing vasodilation
- B Adenosine accumulation during hypoperfusion triggering vasodilation to restore flow
- C Stretch-sensitive (mechanosensitive) ion channels in vascular smooth muscle cells activating upon increased wall tension, causing depolarization and vasoconstriction (Bayliss effect) ✓
- D CO2 accumulation during reduced perfusion stimulating carbonic anhydrase-mediated vasodilation
Explanation
The Bayliss myogenic response is the intrinsic mechanism by which arterial smooth muscle responds to increased transmural pressure by contracting. Stretch-sensitive TRP (transient receptor potential) channels and other mechanosensitive channels in vascular smooth muscle cells depolarize when the vessel wall is stretched by increased intraluminal pressure. This triggers voltage-gated Ca2+ channel opening, Ca2+ influx, and vasoconstriction — precisely opposing the distending force and maintaining constant flow. This explains why CBF remains constant over MAP ~60-150 mmHg. Below 60 mmHg, autoregulation is exhausted (passive vasodilation); above 150 mmHg, breakthrough occurs. CO2 and adenosine are metabolic regulators of CBF, separate from the myogenic mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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