The rate of blood flow entering a capillary network can, in some vascular systems, regulate capillary surface area and the rate of fluid and solute transfer. To determine whether such a mechanism exists in the renal peritubular capillary, we performed micropuncture studies in 28 rats during relatively low and high efferent arteriolar blood flow (EABF). High EABF was achieved by intravenous infusion of isoncotic plasma (group 1: from 120 +/- 11 to 301 +/- 49 nl/min [+/- SE]); whole blood with high hematocrit (approximately 75 vol %) (group 2: from 141 +/- 14 to 252 +/- 31 nl/min); or acetylcholine (group 3: from 193 +/- 20 to 266 +/- 26 nl/min). In group 1 rats, plasma infusion caused an increase in single nephron glomerular filtration rate (SNGFR), on average, from 23.2 +/- 2.4 to 45.2 +/- 3.9 nl/min, owing primarily to increased glomerular plasma flow rate (from 63 +/- 5 to 210 +/- 21 nl/min). The rate of fluid uptake by the peritubular capillary, assessed by the absolute rate of proximal fluid reabsorption (APR), also rose significantly, on average from 10.5 +/- 1.2 to 17.5 +/- 2.4 nl/min. This rise in APR was associated with near constancy in mean transcapillary hydraulic (delta Pc) and oncotic (delta IIc) pressure differences, and was therefore attributed to a significant increase in peritubular capillary reabsorption coefficient (Kr), with the mean from 0.017 +/- 0.003 to 0.030 +/- 0.005 nl/(s . mmHg). In group 2 rats, high hematocrit blood infusion led to a significant rise in APR; on average, from 10.7 +/- 0.7 to 15.0 +/- 1.2 nl/min, without changing SNGFR. This rise in APR occurred despite unfavorable changes in the physical forces, namely a significant increase in delta Pc and constancy in delta IIc. Instead, an increase in EABF was again associated with a significant rise in Kr (on average, from 0.016 +/- 0.002 to 0.030 +/- 0.06 nl/[s . mmHg]), which accounted entirely for the rise in APR, independently of SNGFR. In group 3 rats, in which an increase of EABF was induced pharmacologically with acetylcholine, a rise in EABF was also accompanied by a significant increase in Kr, on average, from 0.019 +/- 0.002 to 0.026 +/- 0.004 nl/(s . mmHg). The results indicate that: (a) Kr is modulated by EABF. (b) In view of plasma flow dependence of GFR, blood flow dependence of Kr and APR provides an important basis for glomerulotubular balance.