GFR Autoregulation: Afferent/Efferent Arteriolar Dynamics

Glomerular filtration rate (GFR) is determined by the net filtration pressure across the glomerular capillary, which depends on the balance of hydrostatic and oncotic pressures (Starling forces) and the glomerular filtration coefficient. The kidney maintains stable GFR across a wide range of systemic blood pressures (MAP 80-180 mmHg) through two intrinsic autoregulatory mechanisms: (1) Myogenic response — afferent arteriolar smooth muscle contracts in response to increased pressure (stretch-activated calcium channels) and relaxes with decreased pressure, maintaining constant glomerular capillary pressure; (2) Tubuloglomerular feedback (TGF) — the macula densa of the juxtaglomerular apparatus senses sodium chloride concentration in the distal tubule filtrate. High NaCl delivery (indicating excessive GFR) triggers adenosine release, causing afferent arteriolar constriction to reduce GFR. Low NaCl delivery stimulates renin release from juxtaglomerular cells, activating RAAS and constricting the efferent arteriole to maintain GFR. ACE inhibitors and ARBs dilate the efferent arteriole, reducing intraglomerular pressure — this is renoprotective in CKD and diabetic nephropathy (reduces proteinuria and slows progression) but can precipitate AKI if renal perfusion is critically dependent on efferent tone (bilateral renal artery stenosis, severe heart...