efferent arteriole

The efferent arteriole arises from the glomerular capillary network within Bowman's capsule and carries filtered blood downstream to either the peritubular capillaries (cortical nephrons) or the vasa recta (juxtamedullary nephrons). Unlike most vascular beds, the kidney has two arteriolar resistance vessels in series (afferent and efferent), allowing independent regulation of glomerular hydrostatic pressure and thus GFR.

Physiologically, efferent arteriolar tone is a key determinant of glomerular filtration pressure. Constriction of the efferent arteriole (mediated primarily by angiotensin II) increases glomerular hydrostatic pressure and helps preserve GFR despite decreased renal blood flow, such as in hypovolemia or renal artery stenosis. This is the pharmacologic basis for why ACE inhibitors and ARBs, which block angiotensin II's vasoconstrictive effect on the efferent arteriole, can precipitate acute kidney injury in patients with bilateral renal artery stenosis—efferent dilation drops GFR significantly.

In contrast, afferent arteriolar constriction (e.g., from NSAIDs blocking prostaglandins) decreases GFR by reducing renal blood flow into the glomerulus. Understanding the balance between afferent and efferent arteriolar tone is essential for understanding renal autoregulation (myogenic mechanism and tubuloglomerular feedback), the effects of drugs (ACEi/ARBs, NSAIDs, calcineurin inhibitors) on renal function, and pathologic states like prerenal azotemia.

Clinically, efferent arteriole physiology is tested extensively in questions about the renin-angiotensin-aldosterone system (RAAS), drug-induced changes in GFR (filtration fraction), and the pathophysiology of diabetic nephropathy, where efferent arteriolar constriction from long-standing hyperglycemia contributes to glomerular hyperfiltration and injury.