Abstract
Abstract
We performed paired series of stop-flow studies on six mongrel dogs to determine a possible nephron site of action of synthetic atrial natriuretic factor (ANF). The initial free-flow response to intrarenal infusion of 5 μg/min of synthetic ANF into mannitol-expanded dogs resulted in an increased urine flow rate (6.81 ± 0.88 to 9.00 ± 1.17 ml/min, P < 0.05) and a 40% increase in sodium excretion (496 ± 110 to 694 ± 166 meq/min, P < 0.025) when compared to paired control periods. Renal blood flow did not change, but the glomerular filtration rate increased 4% (47 ± 5 to 49 ± 6 ml/min, P < 0.05). The filtered load of sodium increased 4% (P < 0.05), and the fractional sodium excretion increased by 35% (P < 0.01). Stop-flow experiments showed no difference in tubular sodium concentration or in the fractional sodium-to-inulin ratio at the nadir of sodium concentration, suggesting that no differences existed in distal tubular sodium handling. Further, no apparent differences were detected in collections representing the more proximal portions of the nephron. While we were able to demonstrate marked natriuresis in response to synthetic ANF, no tubular effect was discernible, and the natriuresis obtained appears to be predominantly a function of hemodynamic effects.
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