&NA;Pressure‐diameter relations were studied in rat afferent arterioles using an isolated, juxtamedullary nephron preparation perfused with a saline solution containing 5% albumin. Angiotensin I (10 &mgr;M), angiotensin II (0.1 &mgr;M), and norepinephrine (10 &mgr;M) increased perfusion pressure, and norepinephrine, but not angiotensin I or II, contracted afferent arterioles, indicating that the vessels are reactive. The control diameter of the afferent arterioles that exhibited pressure‐dependent contraction (n=58) averaged 30.8±1.1 &mgr;m at perfusion pressure of 80 mm Hg. When pressure was increased from 80 to 120 and then to 180 mm Hg, the diameter of these arterioles decreased by 16.4±2.1%. Glomerular capillary pressure was well autoregulated and averaged 45.2±2.2, 50.2±2.4, and 53.0±3.0 mm Hg, respectively, at perfusion pressures of 80, 120, and 180 mm Hg. Administration of vasodilators or a Ca2+‐free solution eliminated the contractile response to pressure elevations; rather, the diameter of these vessels increased significantly by 17.5±5.1% and 32.0±9.4%, respectively, when pressure was increased from 80 to 180 mm Hg. Blocking tubuloglomerular feedback mechanism, with furosemide or by removal of the renal papilla (which interrupts the delivery of fluid to the macula densa), eliminated the pressure‐dependent contraction of the afferent arterioles. Instead the diameter of these vessels increased by 27.0±7.8% and 36.0±5.6%, respectively, when the pressure was increased from 80 to 120 and then to 180 mm Hg. These results demonstrate that juxtamedullary nephrons perfused in vitro autoregulate glomerular capillary pressure. This effect is mediated via a contraction of the terminal portion of afferent arterioles and is dependent on the tubuloglomerular feedback mechanism. (Circulation Research1989;64:790‐798)