Abstract
Abstract
The mechanisms by which atrial natriuretic peptide (ANP) produces a diuresis and natriuresis remain unclear. It has been suggested that the major if not sole mediator of ANP's renal effects is a hemodynamically induced increase in glomerular filtration rate (GFR). Data from clearance studies in anesthetized rabbits demonstrate that ANP administration can produce a significant increase in absolute and percentage sodium excretion (42.0 ± 5.9 → 64.6 ± 10.2 μeq/min, P < 0.01, and 1.97 ± 0.28 → 3.12 ± 0.35%, P < 0.001, respectively) without increasing GFR (16.8 ± 2.1 → 16.1 ±2.5 cc/min, P > 0.30). The natriuresis occurred despite a fall in renal plasma flow (RPF) (56.7 ± 7.0 → 44.5 ± 9.4 cc/min, P < 0.01), a rise in filtration fraction (0.33 ± 0.01 → 0.46 ± 0.05, P < 0.01), and an unchanged filtered load of sodium (2.28 ± 0.27 → 2.16 ± 0.32 μeq/min, P > 0.10). Isolated tubular microperfusion studies demonstrated that ANP, present as a 10−9 M concentration in the solution bathing perfused proximal straight tubules (PST), did not affect fluid flux (J v) (0.38 ± 0.07 → 0.41 ± 0.07 nl/mm/min, P > 0.30) or phosphate reabsorption (J p) (1.50 ± 0.5 → 1.38 ± 0.36 pmole/mm/min, P > 0.50). When ANP was infused into rabbits prior to harvesting the PSTs for isolated tubular microperfusion and the results were compared to tubules taken from control animals, there was again no effect on J v (0.37 ± 0.05 vs 0.42 ± 0.05 nl/mm/min, P > 0.50) or J p (2.41 ± 0.27 vs 2.42 ± 0.44 pmole/mm/min, P > 0.90). These findings suggest that ANP can inhibit sodium transport without increasing whole-kidney GFR or RPF, but does not directly inhibit transport in the proximal straight tubule.
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