刺激脑内渗透压感受器能降低大鼠管球反馈的敏感性

STIMULATION OF THE BRAIN OSMORECEPTOR ATTENUATES THE SENSITIVITY OF TUBULO-GLOMERULAR FEEDBACK IN RATS

在麻醉大鼠肾脏近曲小管和远曲小管分别进行微穿刺,采集小管液。测定单个肾单位肾小球滤过率(SNGFR)。由于微穿刺部位对管球反馈造成的影响,在同一肾单位,采集近曲小管末段小管液测出的SNGFR值(SNGFR_p)比在远曲小管起始段测出的SNGFR值(SNG-FR_d)高,故可将在这两个部位测得的SNGFR值的差(SNGFR_(p-d))用作衡量管球反馈(TGF)敏感性的间接指标。脑室内注射高张盐水(icv.HS)后,SNGFR_(p-d)减小,表明脑内渗透压感受器受刺激可使TGF的敏感性降低。静脉注射速尿后,icv.HS不再引起肾血浆流量和肾小球滤过率的增加,但仍能引起尿钠排出增多。上述结果表明,刺激脑内渗透压感受器可通过减弱TGF导致肾脏血流动力学的改变,而其增加尿钠排出的效应则是通过抑制肾小管的重吸收实现的。

By using micropuncture technique and measuring inulin concentrations inplasma and tubular fluid, and tubular flow rate, single nephron glomerular flltra-tion rate (SNGFR) was calculated. The effect of stimulation of the brain osmorece-ptors on the sensitivity of tubulo-glomerular feedback in rats was observed.The SNGFR value measured at the proximal tubular (SNGFR_p) was greater thanthat measured at the distal tubule (SNGFR_d) of the same nephron. The differe-nce between these two values (SNGFR_(p-d)) was a measure of the extent of tubu-loglomerular feedback (TGF). The SNGFR_(p-d) value was reduced after intracere-broventricular administration of hypertonic saline (icv. HS), indicating that stim-ulation of the brain osmoreceptor can attenuate the sensitivity of TGF. The icv.HS-induced increase in renal plasma flow rate and glomerular filtration rate couldbe abolished by intravenous injection of furosemide, while natriuretic responsepersisted. These results suggest thaticv. HS can alter renal hemodynamics viareduction of TGF, and confirm the claim that icv. HS can inhibit tubular rea-bsorption, which is responsible for the natriuretic response.