Bacon R A, Wu K I, Ying A L, Kempson S A
Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis.
Biochim Biophys Acta. 1987 Dec 11;905(2):268-72. doi: 10.1016/0005-2736(87)90454-8.
Nicotinamide, like parathyroid hormone, is a rapidly acting specific inhibitor of Na+-dependent transport of phosphate (Pi) across the brush-border membrane of the proximal tubule of the mammalian kidney. Pretreatment of rats with colchicine (0.7 mg/kg body weight) for 1 h led to a significantly diminished phosphaturic response to parathyroid hormone (synthetic 1-34 fragment, 4 micrograms/kg). In contrast, the same dose of colchicine had no effect on the renal response to nicotinamide (1.0 g/kg), measured both as the change in urinary Pi excretion and as Na+-dependent Pi uptake by isolated brush-border membrane vesicles. These data suggest indirectly that the intracellular mechanism that mediates the inhibitory effects of nicotinamide on renal Pi transport does not require intact microtubules.
烟酰胺与甲状旁腺激素一样,是一种作用迅速的特异性抑制剂,可抑制哺乳动物肾脏近端小管刷状缘膜上钠依赖性磷酸盐(Pi)的转运。用秋水仙碱(0.7毫克/千克体重)预处理大鼠1小时,可导致对甲状旁腺激素(合成的1 - 34片段,4微克/千克)的磷尿反应显著减弱。相比之下,相同剂量的秋水仙碱对烟酰胺(1.0克/千克)的肾脏反应没有影响,这一反应通过尿Pi排泄变化和分离的刷状缘膜囊泡对钠依赖性Pi摄取来衡量。这些数据间接表明,介导烟酰胺对肾脏Pi转运抑制作用的细胞内机制不需要完整的微管。