Burnett J C, Opgenorth T J, Granger J P
Kidney Int. 1986 Jul;30(1):16-9. doi: 10.1038/ki.1986.144.
Studies were performed in anesthetized dogs (N = 7) to determine the effects of synthetic atrial natriuretic peptide (ANP) on sodium excretion in the presence and absence of control of glomerular filtration rate produced by suprarenal aortic clamping. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms/kg/min) significantly increased glomerular filtration rate from 29.3 +/- 3.0 to 43.2 +/- 4.4 ml/min, urinary sodium excretion from 20.1 +/- 10.3 to 223.3 +/- 52.3 microEq/min, fractional sodium excretion from 0.47 +/- 0.19 to 3.75 +/- 0.59%. In contrast, aortic clamping blocked the increase in glomerular filtration rate in association with an attenuated natriuresis. Urinary sodium excretion increased from 6.3 +/- 2.3 to 68.3 +/- 23.4 microEq/min and fractional sodium excretion increased from 0.15 +/- 0.04 to 0.90 +/- 0.30%. Despite this differential response in glomerular filtration rate and sodium excretion, whole kidney fractional delivery of sodium from the proximal tubule as estimated by the fractional excretion of lithium increased during both unclamped (17.7 +/- 1.8 to 30.4 +/- 0.8%) and clamped (12.9 +/- 2.1 to 23.9 +/- 2.7%) periods. These studies demonstrate that atrial natriuretic peptide-induced natriuresis is importantly mediated by an increase in glomerular filtration rate and decrease in tubular reabsorption.
对7只麻醉犬进行研究，以确定在存在和不存在由肾上主动脉夹闭控制肾小球滤过率的情况下，合成心房利钠肽（ANP）对钠排泄的影响。肾内输注合成心房利钠肽（0.3微克/千克/分钟）可使肾小球滤过率从29.3±3.0显著增加至43.2±4.4毫升/分钟，尿钠排泄从20.1±10.3显著增加至223.3±52.3微当量/分钟，钠排泄分数从0.47±0.19显著增加至3.75±0.59%。相比之下，主动脉夹闭会阻止肾小球滤过率的增加，并伴有利钠作用减弱。尿钠排泄从6.3±2.3增加至68.3±23.4微当量/分钟，钠排泄分数从0.15±0.04增加至0.90±0.30%。尽管在肾小球滤过率和钠排泄方面存在这种差异反应，但在未夹闭（17.7±1.8至30.4±0.8%）和夹闭（12.9±2.1至23.9±2.7%）期间，通过锂排泄分数估计的近端小管钠的全肾分数输送均增加。这些研究表明，心房利钠肽诱导的利钠作用主要由肾小球滤过率增加和肾小管重吸收减少介导。
