Cerebral blood flow (CBF) is tightly autoregulated between mean arterial pressures of 60 and 160 mmHg. In chronic hypertension, this autoregulatory range is shifted to the right. What is the primary mechanism of myogenic autoregulation of cerebral vessels?

• A Increased transmural pressure stretches cerebrovascular smooth muscle, directly activating mechanosensitive (Bayliss) channels (TRPC/TRPM) leading to membrane depolarisation, Ca²⁺ influx via voltage-gated Ca²⁺ channels, and vasoconstriction ✓
• B Rising pressure increases cerebral blood flow, delivering more O2 and reducing adenosine release, which removes vasodilatory tone
• C Increased transmural pressure stretches endothelial cells, which release nitric oxide to dilate cerebral arteries and maintain constant flow
• D Baroreceptors in the Circle of Willis detect pressure changes and activate sympathetic vasoconstrictor fibres to cerebral resistance arteries

Explanation

Myogenic (Bayliss) autoregulation is intrinsic to vascular smooth muscle: stretch from increased transmural pressure activates mechanosensitive cation channels (including members of the TRP family), causing membrane depolarisation; this opens voltage-gated L-type Ca²⁺ channels, increasing intracellular Ca²⁺ and triggering smooth muscle contraction—vasoconstriction that reduces flow back toward baseline. In chronic hypertension, smooth muscle hypertrophies and the mechanical threshold for constriction resets to higher pressures, explaining the rightward shift. Option B describes metabolic autoregulation (adenosine/CO2-based), not myogenic. Endothelial NO is vasodilatory and opposes, rather than mediates, myogenic constriction. Cerebral vessels have sparse sympathetic innervation and no intrinsic baroreceptors.

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

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