afferent arteriole

The afferent arteriole is part of the renal microvasculature supplying blood to the glomerulus, where filtration of plasma begins to form the ultrafiltrate. It arises from the interlobular arteries and branches into the glomerular capillary tuft, which then drains into the efferent arteriole (unusual anatomy where a capillary bed is between two arterioles).

Physiologically, the afferent arteriole plays a central role in renal autoregulation via two mechanisms: (1) the myogenic mechanism, where increased pressure/stretch causes vascular smooth muscle contraction to maintain constant RBF and GFR, and (2) tubuloglomerular feedback, part of the juxtaglomerular apparatus, where increased NaCl delivery to the macula densa triggers afferent arteriolar constriction (via adenosine) to reduce GFR, protecting against excessive filtration.

The afferent arteriole's smooth muscle cells transform into juxtaglomerular (JG) cells, which sense a decrease in perfusion pressure and secrete renin, activating the renin-angiotensin-aldosterone system (RAAS) to help regulate blood pressure and fluid balance.

Clinically, the afferent arteriole is affected by: - NSAIDs: inhibit prostaglandins, which normally dilate the afferent arteriole; NSAID use can cause afferent arteriole constriction, decreasing GFR (risk of acute kidney injury, especially in volume-depleted states). - Hyaline arteriolosclerosis (seen in diabetes mellitus and hypertension): affects afferent > efferent arteriole, causing glomerular ischemia. - Prostaglandins and dopamine dilate the afferent arteriole, increasing renal blood flow and GFR. - In contrast, ACE inhibitors/ARBs act primarily on the efferent arteriole (vasodilation), decreasing GFR — useful in diabetic nephropathy to reduce intraglomerular pressure.

Understanding the difference in afferent vs. efferent arteriole responses to drugs and pathology is a classic USMLE topic, especially regarding changes in renal blood flow, GFR, and filtration fraction.