【摘要】 实验在麻醉大鼠上进行。用肾小管微穿刺技术观察到,脑室内注射高张盐水（icv.HS）后:（1）近曲小管末段钠残留分数从53.0±2.1％升高至66.0±2.9％（P<0.01）;氯残留分数从65.4±3.4％升高至78.2±3.9％（P<0.05）;钾残留分数和小管液渗透克分子浓度无显著变化。（2）远曲小管起始段钠残留分数从8.2±0.9％升高至13.6±1.8％（P<0.05）;氯残留分数从5.4±0.8％升高至9.5±1.4％（P<0.05）;小管液渗透克分子浓度从139.8±6.9mOsm/kg H₂O升高至181.3±15.6mOsm/kgH₂O（P<0.05）;钾残留分数无显著变化。静脉注射速尿能消除icv.HS引起的尿钾增多反应,但不能消除icv.HS引起的利尿和尿钠增多反应。上述结果表明,刺激脑内渗透压感受器能抑制近曲小管中钠和氯的重吸收,并促进远曲小管及其以后部位的钠钾交换,导致尿钠排出增多和尿钾排出增多。更多还原

【Abstract】 The tubular reabsorption of sodium, chloride and potassium was studiedwith micropuncture technique and electron probe X-ray microanalysis before andfollowing intracerebroventricular administration of hypertonic saline （icv. HS）in rats. At the late proximal convoluted tubules, the fractional delivery of sodiumincreased from 53.0±2.1% to 66.0±2.9% （P<0.01）, the fractional delivery ofchloride increased from 65.4±3.4% to 78.2±3.9% （P<0.05）, but the fractionaldelivery of potassium and tubular fluid osmolality were unaltered. At the earlydistal convoluted tubules, the fractional delivery of sodium increased from 8.2±0.9% to 13.6±1.8% （P<0.05）, the fractional delivery of chloride increasedfrom 5.4±0.8% to 9.5±1.4% （P<0.05）, the tubular fluid osmolalityincreased from 139.8±6.9 mOsm/kg H₂O to 181.3±15.6 mOsm/kg H₂O,whereas fractional delivery of potassium did not show significant change. Underthe condition of diuresis provoked by the intravenous administration of furosemidethe kaliuresis induced by icv. HS was abolished, while the icv. HS-eliciteddiuresis and natriuresis remained unaffected. These results indicate that stimula-tion of the brain osmoreceptor inhibits the proximal tubular reabsorption of sodiumchloride which in turn enhances sodium-potassium exchange in the distal tubulesand collecting ducts.更多还原