The myogenic autoregulation of blood flow in renal and cerebral vessels is due to:
- A Stretching of vascular smooth muscle by increased intraluminal pressure triggers mechanosensitive channels (possibly TRPC channels), causing depolarisation and Ca2+ entry, leading to vasoconstriction (Bayliss effect) ✓
- B Release of local adenosine from metabolically active tissue causing vasodilation proportional to metabolic demand
- C Endothelin-1 released from endothelial cells in response to shear stress causes proportional vasoconstriction to maintain flow
- D The sympathetic nervous system directly mediates myogenic responses via alpha-1 receptor activation in response to pressure changes
Explanation
Myogenic autoregulation (Bayliss effect) is an intrinsic property of vascular smooth muscle. When intraluminal pressure increases, wall tension rises, stretching mechanosensitive cation channels (including TRPC1/6 and ENaC-like channels) in the smooth muscle membrane. This causes membrane depolarisation, activation of voltage-gated L-type Ca2+ channels, Ca2+ influx, and resultant vasoconstriction. This response is independent of neural or humoral input, occurring even in denervated isolated vessels. In the kidney, myogenic autoregulation is critical to maintain GFR over MAP 80–160 mmHg. In the brain, it maintains constant CBF over MAP 50–150 mmHg. Adenosine (option B) is a metabolic vasodilator, not a myogenic mechanism. Endothelin-1 (option C) is a potent vasoconstrictor but responds to different stimuli. Sympathetic nerves (option D) are not required for the myogenic response.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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