刺激脑内渗透压感受器对大鼠肾小管重吸收钠,氯,钾的影响

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 H_2O升高至181.3±15.6mOsm/kgH_2O(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。

THE EFFECTS OF STIMULATION OF THE BRAIN OSMORECEPTOR ON THE TUBULAR REABSORPTION OF SODIUM, CHLORIDE AND POTASSIUM IN RATS

The tubular reabsorption of sodium, chloride and potassium was studied with micropuncture technique and electron probe X-ray microanalysis before and following intracerebroventricular administration of hypertonic saline (icv. HS) in rats. At the late proximal convoluted tubules, the fractional delivery of sodium increased from 53.0 +/- 2.1% to 66.0 +/- 2.9% (P < 0.01), the fractional delivery of chloride increased from 65.4 +/- 3.4% to 78.2 +/- 3.9% (P < 0.05), but the fractional delivery of potassium and tubular fluid osmolarity were unaltered. At the early distal 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 increased from 5.4 +/- 0.8% to 9.5 +/- 1.4% (P < 0.05), the tubular fluid osmolality increased from 139.8 +/- 6.9 mOsm/kg H2O to 181.3 +/- 15.6 mOsm/kg H2O2 whereas fractional delivery of potassium did not show significant change. Under the condition of diuresis provoked by the intravenous administration of furosemide the kaliuresis induced by icv. HS was abolished, while the icv. HS-elicited diuresis and natriuresis remained unaffected. These results indicate that stimulation of the brain osmoreceptor inhibits the proximal tubular reabsorption of sodium chloride which in turn enhances sodium-potassium exchange in the distal tubules and collecting ducts.