DIETARY SALT EXTREMES AND RENAL-FUNCTION IN RATS - EFFECT OF ATRIAL-NATRIURETIC-FACTOR

1. Chronic reduction of salt intake can reduce the natriuretic effect of exogenously administered atrial natriuretic factor. The purpose of this study was to elucidate the intrarenal site(s) of such atrial natr iuretic factor resistance. Renal clearance and collecting duct microca theterization experiments were made before and during infusion of atri al natriuretic factor in three groups of rats: group 1 consisted of ra ts fed a high salt diet (8% NaCl) for 1 week before the experiment; gr oup II were fed a low salt diet (< 0.008%); group III received the sam e low salt diet, but were acutely replenished with salt at the time of experiment. 2. Baseline sodium chloride excretion was 6480 +/- 810 nm ol min(-1) g(-1) kidney weight in group 1 compared to 99 +/- 16 in gro up 1. Fractional reabsorptions in the medullary collecting duct were 3 7 +/- 6% and 95 +/- 2% of delivered load, respectively (P < 0.05). The fractions of filtered sodium remaining at the beginning of the medull ary duct were 6.6 +/- 1.0% of filtered load in group 1 and 2.7 +/- 0.7 % in group II (P < 0.05), indicating increased tubular reabsorption in group II, not only in the medullary duct, but also in upstream nephro n segments. 3. During infusion of atrial natriuretic factor, marked sa luresis (13 240 +/- 750 nmol min(-1) g(-1) kidney weight), together wi th decreased fractional reabsorption at both sites (duct, -13 +/- 9%; upstream remainder, 7.9 +/- 0.7%; P < 0.05 each, compared to correspon ding control values) was found in group 1, whereas the excretory (150 +/- 28 nmol min(-1) g(-1) kidney weight), and the tubular transport (d uct = 84 +/- 3%; upstream remainder = 2.2 +/- 0.4%) changes were quant itatively insignificant in group II. Glomerular filtration rate was in creased in group 1 from 1.07 +/- 0.03 to 1.26 +/- 0.04 ml min(-1) g(-1 ) kidney weight (P < 0.05), but not in group II (0.93 +/- 0.07 to 0.96 +/- 0.09, not significant). 4. In group III, acute salt replenishment was associated with increased excretion (1940 +/- 440 nmol min(-1) g( -1) kidney weight, P < 0.05 compared to group II) and with reduction o f tubular reabsorption in the collecting duct only (69 +/- 8%, P < 0.0 5). Infusion of atrial natriuretic factor in this group further increa sed natriuresis (7810 +/- 780 nmol min(-1) g(-1) kidney weight) and de creased tubular reabsorption in the duct (-32 +/- 22%, P < 0.05 compar ed to the corresponding control value). 5. We conclude that chronic sa lt deprivation can effectively prevent, via a rapidly reversible count erregulatory mechanism, the expected actions of atrial natriuretic fac tor on sodium reabsorption in the medullary collecting duct. Operation of such mechanism may explain salt retention despite elevated endogen ous levels of atrial natriuretic factor in pathological states such as congestive heart failure and liver cirrhosis.