The myogenic response of arterioles (Bayliss effect) enables pressure autoregulation in the cerebral and renal circulations. The molecular mechanism involves:

• A Increased pressure activates endothelial nitric oxide synthase → excess NO → cGMP-mediated vasoconstriction
• B Stretch activates phospholipase A2 → arachidonic acid → thromboxane A2 → TP receptor-mediated contraction
• C Increased intraluminal pressure → stretch-activated non-selective cation channels (TRPC6/TRPM4) → depolarization → CaV1.2 L-type channel activation → vasoconstriction ✓
• D Elevated pressure inhibits Na⁺/K⁺-ATPase → elevated intracellular Na⁺ → reversed NCX → Ca²⁺ loading → vasoconstriction

Explanation

The myogenic (Bayliss) response is an intrinsic property of vascular smooth muscle: increased intraluminal pressure causes vasoconstriction and decreased pressure causes vasodilation. Mechanosensitive stretch-activated ion channels, particularly TRPC6 (transient receptor potential canonical 6) and TRPM4, depolarize the smooth muscle cell in response to wall stretch. This depolarization activates voltage-gated L-type Ca²⁺ channels (CaV1.2), causing Ca²⁺ influx, myosin light-chain kinase (MLCK) activation, and contraction. This mechanism is essential for cerebral and renal autoregulation, maintaining constant blood flow over a MAP range of approximately 60–160 mmHg.

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

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