The relative contributions of AT_1A and AT_1B receptors to afferent arteriolar autoregulatory capability and afferent and efferent arteriolar responses to ANG II are not known. Experiments were conducted in kidneys from wild-type (WT) and AT_1A−/− mice utilizing the in vitro blood-perfused juxtamedullary nephron technique. Direct measurements of afferent (AAD) and efferent arteriolar diameters (EAD) were assessed at a renal arterial pressure of 100 mmHg. AAD averaged 14.8 ± 0.8 μm for WT and 14.9 ± 0.8 μm for AT_1A−/− mice. AAD significantly decreased by 7 ± 1, 16 ± 1, and 26 ± 2% for WT mice and by 11 ± 1, 20 ± 2, and 30 ± 3% for AT_1A−/− mice (120, 140, 160 mmHg). AAD autoregulatory capability was not affected by the absence of AT_1A receptors. AAD responses to 10 nM ANG II were significantly blunted for AT_1A−/− mice compared with WT (−22 ± 2 vs. −37 ± 5%). ANG II (0.1–10 nM) failed to elicit any change in EAD for AT_1A−/− mice. AAD and EAD reductions in ANG II were blocked by 1 μM candesartan. We conclude that afferent arteriole vasoconstrictor responses to ANG II are mediated by AT_1A and AT_1B receptors, whereas efferent arteriolar vasoconstrictor responses to ANG II are mediated by only AT_1A receptors in the mouse kidney.