Mercier O, Bichara M, Delahousse M, Prigent A, Leviel F, Paillard M
Laboratoire de Physiologie et Physiopathologie Rénale et Electrolytique, Université Paris VII, Hôpital Louis Mourier, Colombes, France.
Am J Physiol. 1989 Dec;257(6 Pt 2):F1003-14. doi: 10.1152/ajprenal.1989.257.6.F1003.
Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.
在输注生长抑素且血容量扩张的大鼠中进行了配对微穿刺实验，以研究输注胰高血糖素（0.05 ng·min⁻¹·g体重⁻¹）对尿液酸化及肾小管对碳酸氢盐处理的影响。胰高血糖素对全肾和单肾单位肾小球滤过率无影响。在甲状腺甲状旁腺切除（TPTX）的大鼠中，胰高血糖素抑制了亨利袢中总CO₂的重吸收。然而，在完整动物中未观察到后一种效应。在可进行微穿刺的远端小管中，在血容量扩张加输注生长抑素期间观察到总CO₂的净吸收，而在Wistar大鼠中输注胰高血糖素期间则转变为总CO₂的净分泌；因此，远端小管后期总CO₂的输送增加了近80%。所有动物均出现明显的尿液酸化抑制现象，表现为尿pH值升高和碳酸氢盐排泄增加。相反，输注生长抑素降低了血浆胰高血糖素浓度，刺激了Wistar大鼠远端小管总CO₂的净吸收并增强了最终尿液酸化。最后，在碳酸氢盐负荷的TPTX大鼠中，输注胰高血糖素显著降低了碱性利尿期间尿-血PCO₂。我们得出结论：1）胰高血糖素在TPTX大鼠中抑制浅表亨利袢中碳酸氢盐的吸收，但在完整大鼠中则不然；2）胰高血糖素刺激远端小管和集合管中碳酸氢盐的分泌和/或抑制质子分泌，从而导致尿液酸化减弱。
