Sonnenberg H, Honrath U, Wilson D R
Department of Physiology, University of Toronto, Ont., Canada.
Can J Physiol Pharmacol. 1990 Mar;68(3):402-7. doi: 10.1139/y90-056.
The role of the medullary collecting duct in pressure natriuresis has not been established. In vivo microcatheterization was used to study the effect of an acute increase in blood pressure induced by bilateral carotid artery and vagal nerve ligation on medullary collecting duct function in anaesthetized rats. Increased fluid and electrolyte excretion during pressure natriuresis were accompanied by increased delivery of water, sodium, chloride, and potassium to the beginning of the medullary collecting duct, a change that was significantly greater than in a second series of time-control animals. These increases in delivery were within the range for which constant fractional NaCl reabsorption had been found previously. However, during increased perfusion pressure, reabsorption of both sodium and chloride in the medullary collecting duct as a fraction of delivered load were reduced from 81 +/- 4.1 to 51 +/- 9.3% (p less than 0.01) and from 65.7 +/- 6.0 to 42.7 +/- 9.1% (p less than 0.01), respectively. No significant changes in medullary collecting reabsorption were seen in the time controls. We conclude that increased perfusion pressure, in addition to increasing delivery to the medullary collecting duct, also inhibits sodium chloride reabsorption in this nephron segment.
髓质集合管在压力性利钠中的作用尚未明确。采用体内微导管插入术研究双侧颈动脉和迷走神经结扎引起的血压急性升高对麻醉大鼠髓质集合管功能的影响。压力性利钠期间液体和电解质排泄增加，同时输送到髓质集合管起始部的水、钠、氯和钾增多，这一变化明显大于第二组时间对照动物。这些输送量的增加处于先前发现的氯化钠重吸收分数恒定的范围内。然而，在灌注压升高期间，髓质集合管中钠和氯作为输送负荷的一部分的重吸收分别从81±4.1%降至51±9.3%（p<0.01）和从65.7±6.0%降至42.7±9.1%（p<0.01）。时间对照中髓质集合管重吸收未见明显变化。我们得出结论，灌注压升高除了增加向髓质集合管的输送外，还抑制该肾单位节段的氯化钠重吸收。
