Renal autoregulation
Also known as: autoregulation of GFR, myogenic response, tubuloglomerular feedback, TGF
Intrinsic mechanisms — the myogenic response and tubuloglomerular feedback — that keep renal blood flow and GFR nearly constant over a mean arterial pressure of ≈80–180 mmHg.
Overview
Myogenic mechanism: a rise in arterial pressure stretches the smooth muscle of the afferent arteriole, opening stretch-activated cation channels → depolarisation → Ca²⁺ entry → contraction, which raises resistance and keeps glomerular pressure and flow steady; a fall in pressure does the reverse. It is fast (seconds) and protects the glomeruli from hypertensive injury.
Tubuloglomerular feedback (TGF): if GFR rises, more NaCl reaches the macula densa, which releases ATP/adenosine → afferent arteriolar constriction (A1 receptors) → GFR falls back; low NaCl delivery dilates the afferent arteriole and stimulates renin, whose angiotensin II then constricts the efferent arteriole to support GFR. TGF matches each nephron's filtered load to the reabsorptive capacity of its tubule.
Autoregulation is not perfect and fails below a MAP of ≈70–80 mmHg (shock), when GFR and urine output fall steeply. Strong sympathetic activation (haemorrhage, exercise) overrides it, constricting afferent arterioles to divert blood to vital organs.
- Location
Afferent arterioles and juxtaglomerular apparatus.
Function
- Stabilise GFR and renal blood flow despite blood pressure changes
- Protect glomeruli from high pressures
- Match filtered load to tubular reabsorptive capacity
- Physiology
Autoregulatory range ≈80–180 mmHg MAP. Pressure natriuresis persists despite autoregulation and is central to long-term blood pressure control.
Clinical significance
Impaired autoregulation
Ageing, chronic hypertension, CKD and diabetes shift or blunt autoregulation; NSAIDs and ACE inhibitors impair the prostaglandin and angiotensin II components, making the kidney vulnerable to hypotension.
Test yourself
The macula densa regulates afferent arteriolar tone (tubuloglomerular feedback) by sensing:
- Afferent arteriolar wall stretch
- NaCl concentration of tubular fluid at the end of the thick ascending limb
- Plasma osmolality
- Plasma K⁺ concentration
Answer: NaCl concentration of tubular fluid at the end of the thick ascending limb
Macula densa cells take up NaCl via NKCC2. High NaCl delivery (high GFR) → ATP/adenosine release → A1-receptor-mediated afferent constriction → GFR falls; low NaCl → afferent dilation and renin release.
Compiled from standard anatomy and physiology references — see the Urinary System sources. For education only; not medical advice.