According to myogenic hypothesis of renal autoregulation the afferent arterioles contract in response to stretch – induced by ____________

Correct Answer: C. Opening of calcium channels

The myogenic hypothesis of renal autoregulation explains how the kidney maintains stable glomerular filtration rate (GFR) despite fluctuations in systemic blood pressure. When blood pressure increases, the afferent arteriole wall experiences increased transmural pressure and stretch. This mechanical stretch activates stretch-sensitive ion channels (mechanoreceptors) in the smooth muscle cells of the afferent arteriole. The opening of these calcium channels allows Ca²⁺ influx into the vascular smooth muscle cells, triggering depolarization and subsequent contraction of the afferent arteriole. This vasoconstriction reduces glomerular capillary pressure and maintains GFR within a narrow range (typically 80–180 mmHg mean arterial pressure). Conversely, decreased blood pressure reduces stretch, calcium channel opening decreases, and the afferent arteriole dilates. This mechanism is intrinsic to the kidney and does not require neural or hormonal input—it is a purely mechanical response of the vascular smooth muscle. The myogenic response is the primary autoregulatory mechanism in the kidney and operates independently of the tubuloglomerular feedback system.

Why the other options are wrong

A. Noradrenaline — Noradrenaline is a sympathetic neurotransmitter that causes vasoconstriction via α₁-adrenergic receptors, but it is NOT the primary trigger for the myogenic response. The myogenic hypothesis is a purely mechanical, intrinsic renal mechanism independent of neural input. Noradrenaline plays a role in renal autoregulation only under extreme stress (mean arterial pressure <80 mmHg), not in the normal stretch-induced response. This is a common trap—confusing neural regulation with the intrinsic myogenic mechanism. B. Adenosine — Adenosine is a metabolic byproduct that causes afferent arteriole vasoconstriction and is part of the tubuloglomerular feedback mechanism (not myogenic autoregulation). Adenosine is released from the macula densa in response to increased sodium chloride delivery, not from stretch of the afferent arteriole. Confusing adenosine with the myogenic response is a classic NBE trap—both regulate GFR, but via different mechanisms and different triggers. D. NO — Nitric oxide (NO) is a vasodilator produced by endothelial cells that causes afferent arteriole dilation and increases GFR. In the myogenic response, NO actually opposes the vasoconstriction triggered by calcium influx. NO is important for maintaining renal perfusion but is not the trigger for stretch-induced contraction. Students may confuse NO's role in vascular tone with the primary mechanism of myogenic autoregulation.

High-Yield Facts

Mnemonics

MYOGENIC = Mechanical + Calcium Mechanical stretch → Calcium channels open → Contraction. Remember: myogenic is purely mechanical (no hormones, no nerves in the primary trigger). Use this when distinguishing myogenic from tubuloglomerular feedback. STRETCH → Ca²⁺ → SQUEEZE STRETCH the afferent arteriole (high BP) → Ca²⁺ channels open → SQUEEZE (vasoconstriction). Opposite happens with low BP: no stretch → no Ca²⁺ → dilation.

NBE Trap

NBE pairs adenosine and myogenic autoregulation to trap students who confuse the two mechanisms. Both regulate GFR, but adenosine is part of tubuloglomerular feedback (macula densa trigger), not the myogenic response (stretch trigger). The question specifically asks about "stretch-induced" response—a red flag that myogenic, not metabolic feedback, is being tested.

Clinical Pearl

In Indian patients with hypertension, the myogenic autoregulation becomes impaired, and the kidney's ability to maintain stable GFR across a wide BP range is lost. This is why aggressive BP control in hypertensive nephropathy is critical—restoring the autoregulatory range prevents further glomerular injury. Conversely, in acute hypotension (sepsis, hemorrhage), loss of myogenic autoregulation below 80 mmHg is why renal perfusion fails rapidly.

_Reference: Guyton & Hall Textbook of Medical Physiology, Ch. 26 (Urine Formation by the Kidney); Harrison's Principles of Internal Medicine, Ch. 279 (Chronic Kidney Disease)_