Cerebral blood flow (CBF) is autoregulated between mean arterial pressures (MAP) of approximately 50–150 mmHg. Which cellular mechanism is primarily responsible for myogenic autoregulation of CBF?

• A Endothelial nitric oxide release triggered by shear stress, causing arteriolar dilation at low MAP
• B Metabolic coupling: CO2 and H+ accumulate when flow is insufficient, directly dilating arterioles via carbonic anhydrase
• C Stretch-activated cation channels in vascular smooth muscle cells causing membrane depolarization and vasoconstriction when transmural pressure rises ✓
• D Adenosine release from astrocytic end-feet detecting inadequate O2 delivery, triggering neurogenic vasodilation

Explanation

Cerebrovascular myogenic autoregulation (Bayliss effect) operates via stretch-activated TRP cation channels (primarily TRPM4/TRPC6) in cerebral arteriolar smooth muscle. When transmural pressure rises, these channels allow Na+/Ca2+ influx → membrane depolarization → L-type Ca2+ channel opening → vasoconstriction, opposing the pressure rise and maintaining CBF. At low MAP, reduced wall tension causes channel closure → hyperpolarization → vasodilation. Metabolic (CO2/H+, adenosine) and flow-mediated (NO) mechanisms contribute to overall regulation but are not the primary myogenic mechanism.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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