Renal autoregulation is mediated by myogenic vasoconstriction and tubuloglomerular feedback. Since defects may contribute to renal barotrauma in salt-sensitive hypertension and chronic kidney disease, we tested the hypothesis that the myogenic response is diminished by dietary salt or the reduced renal mass (RRM). Afferent arterioles (Af) were dissected from 1 2/3 nephrectomized RRM mice and sham-operated controls and perfused during step changes in pressure from 0 to 140 mmHg. The active wall tension (AWT) was the differences between tension measured during perfused with physiologic perfusate and a solution with zero calcium + EGTA. The mean arterial pressure (MAP) of conscious mice by telemetry (108 ± 10 mmHg) was unaffected by salt intake or RRM. Af developed a linear increase in AWT above a perfusion pressure of 60 ± 6 mmHg without plateau. The slope of AWT vs perfusion pressure defined the myogenic response. This response was similar in mice fed normal or high salt for 3 months (3.5±0.3 vs 3.9 ± 0.5 dynes·cm^-1/mmHg, p>0.05). It was unaffected after 3 days or 3 weeks of RRM but reduced by 28±3% and 60±7% (p<0.05) in the normal and high salt RRM groups at 3 months (2.5 ± 0.3 and 1.6 ± 0.3 dynes·cm^-1/mmHg). We conclude that the mouse renal afferent arteriole develops a linear increase in myogenic tone above ambient perfusion pressure. The normal myogenic response is impaired substantially in RRM, especially during high salt intake.