Rybczynska A, Hoppe A, Knox F G
Department of Physiology and Biophysics, Mayo Medical School, Rochester, MN 55905.
J Am Soc Nephrol. 1990 Aug;1(2):200-4. doi: 10.1681/ASN.V12200.
Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone. The decreased phosphaturic response to parathyroid hormone in rats fed a low phosphate diet for 1 day can be restored by propranolol infusion. Free-flow micropuncture studies were performed to localize the nephron site of restoration of the phosphaturic effect of parathyroid hormone by propranolol in rats deprived of phosphate for one day. In animals fed low phosphate diet and in the presence of parathyroid hormone, propranolol infusion did not change phosphate delivery to the late proximal tubule; however, fractional delivery of phosphate to the early distal tubule was significantly increased from 18.3 +/- 2.9 to 32.2 +/- 4.1%. In rats fed a normal phosphate diet, propranolol infusion did not change phosphate delivery along the nephron. We conclude that the restoration of the phosphaturic effect of parathyroid hormone by propranolol infusion in rats deprived of phosphate for 1 day is primarily due to decreased reabsorption of phosphate by superficial loop segments, most likely the pars recta segment of the proximal tubule.
磷缺乏会导致对甲状旁腺激素的利磷作用产生抵抗。给大鼠喂食低磷饮食1天,其对甲状旁腺激素的利磷反应降低,而通过输注普萘洛尔可恢复该反应。进行了自由流微穿刺研究,以定位在缺磷1天的大鼠中普萘洛尔恢复甲状旁腺激素利磷作用的肾单位部位。在喂食低磷饮食且存在甲状旁腺激素的动物中,输注普萘洛尔并未改变向近端小管晚期的磷输送;然而,向远端小管早期的磷分数输送从18.3±2.9%显著增加至32.2±4.1%。在喂食正常磷饮食的大鼠中,输注普萘洛尔并未改变沿肾单位的磷输送。我们得出结论,在缺磷1天的大鼠中,输注普萘洛尔恢复甲状旁腺激素的利磷作用主要是由于浅表袢段(很可能是近端小管的直部段)对磷的重吸收减少。