McGowan J A, Pitts T O, Rose M E, Puschett J B
Proc Soc Exp Biol Med. 1987 May;185(1):62-8. doi: 10.3181/00379727-185-42517.
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 mu eq/min, P less than 0.01, and 1.97 +/- 0.28----3.12 +/- 0.35%, P less than 0.001, respectively) without increasing GFR (16.8 +/- 2.1----16.1 +/- 2.5 cc/min, P greater than 0.30). The natriuresis occurred despite a fall in renal plasma flow (RPF) (56.7 +/- 7.0----44.5 +/- 9.4 cc/min, P less than 0.01), a rise in filtration fraction (0.33 +/- 0.01----0.46 +/- 0.05, P less than 0.01), and an unchanged filtered load of sodium (2.28 +/- 0.27----2.16 +/- 0.32 mu eq/min, P greater than 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 (Jv) (0.38 +/- 0.07----0.41 +/- 0.07 nl/mm/min, P greater than 0.30) or phosphate reabsorption (Jp) (1.50 +/- 0.5----1.38 +/- 0.36 pmole/mm/min, P greater than 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 Jv (0.37 +/- 0.05 vs 0.42 +/- 0.05 nl/mm/min, P greater than 0.50) or Jp (2.41 +/- 0.27 vs 2.42 +/- 0.44 pmole/mm/min, P greater than 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.
心房利钠肽（ANP）产生利尿和利钠作用的机制仍不清楚。有人提出，ANP对肾脏作用的主要（如果不是唯一）介质是血流动力学诱导的肾小球滤过率（GFR）增加。来自麻醉兔清除率研究的数据表明，给予ANP可使绝对钠排泄量和钠排泄百分比显著增加（分别从42.0±5.9----64.6±10.2微当量/分钟，P<0.01，和1.97±0.28----3.12±0.35%，P<0.001），而不增加GFR（从16.8±2.1----16.1±2.5毫升/分钟，P>0.30）。尽管肾血浆流量（RPF）下降（从56.7±7.0----44.5±9.4毫升/分钟，P<0.01）、滤过分数升高（从0.33±0.01----0.46±0.05，P<0.01）和钠滤过负荷不变（从2.28±0.27----2.16±0.32微当量/分钟，P>0.10），利钠作用仍会发生。孤立肾小管微灌注研究表明，在灌注近端直小管（PST）的浴液中以10^(-9)M浓度存在的ANP，不影响液体通量（Jv）（从0.38±0.07----0.41±0.07纳升/毫米/分钟，P>0.30）或磷酸盐重吸收（Jp）（从1.50±0.5----1.38±0.36皮摩尔/毫米/分钟，P>0.50）。当在收获用于孤立肾小管微灌注的PST之前将ANP注入兔体内，并将结果与取自对照动物的肾小管进行比较时，对Jv（0.37±0.05对0.42±0.05纳升/毫米/分钟，P>0.50）或Jp（2.41±0.27对2.42±0.44皮摩尔/毫米/分钟，P>0.90）同样没有影响。这些发现表明，ANP可在不增加全肾GFR或RPF的情况下抑制钠转运，但不会直接抑制近端直小管中的转运。
