Atrial natriuretic factor (ANF) is a peptide originally found to be present in extracts of mammalian atria that possess marked natriuretic and diuretic qualities. A number of mechanisms have been suggested to explain these properties. Recently, it has been suggested that ANF may enhance glomerular filtration. In this report, we describe a series of experiments designed to investigate if atriopeptin II, a 23-amino acid synthetic analogue of ANF, increases glomerular filtration rate (GFR) and, if so, the mechanism for this increase. We used the isolated perfused glomerulus technique (n = 6), which allows a single isolated glomerular unit to be perfused and the determinants of single-nephron GFR (SNGFR) to be measured. Two periods were performed in each experiment, the control followed by the experimental. The only difference between the two periods was the addition of atriopeptin II to the experimental perfusate at a final concentration of 5 X 10(-7) M. There was indeed a significant increase in the SNGFR (78 +/- 27 to 108 +/- 29 nl/min, P less than 0.01). This increase was associated with a significant increase in the glomerular capillary hydrostatic pressure (PGC) from 31 +/- 3 to 35 +/- 3 mmHg (P less than 0.05). The filtration fraction also increased in each experiment (from 0.16 +/- 0.3 to 0.25 +/- 0.03, P less than 0.005). Neither the afferent flow nor the efferent arteriolar flow changed, although there was a tendency for both to decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

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To evaluate the direct effect of albumin concentration on the glomerular capillary ultrafiltration coefficient (Kf), we compared the effect of "normal" (3.4 g/100 ml), "low" (0.1 g/100 ml), and "no albumin" (less than 0.005 g/100 ml) concentration on the determinants of single-nephron glomerular filtration rate (SNGFR) as measured with the isolated perfused glomerulus technique. When the albumin concentration was decreased from normal to low concentrations, the afferent flow rate increased from 318 +/- 147 (mean +/- SE) to 450 +/- 174 nl/min, the filtration fraction increased from 0.19 +/- 0.04 to 0.35 +/- 0.08, and the SNGFR increased from 49 +/- 21 to 126 +/- 34 nl/min. These changes were associated with a small though significant increase in Kf from 2.79 +/- 1.01 to 3.74 +/- 0.98 nl/(min X mmHg) (P less than 0.05). When the albumin concentration was decreased from low to no albumin the filtration fraction and SNGFR increased even further and were associated with a marked increase in Kf to a value of 27.04 +/- 11.43 nl/min X mmHg). We conclude that there is very little effect of decreases in albumin concentration on Kf until extremely low levels are reached, and at that point there is a marked increase in the ultrafiltration coefficient. Furthermore, when these extremely low concentrations of albumin are reached an important role for albumin in the basic function of the ultrafiltration barrier is demonstrable.

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