Damasco M C, Malnic G
Miner Electrolyte Metab. 1987;13(1):26-32.
The role of corticosteroid hormones in proximal tubular acidification was studied in control, sham-operated and adrenalectomized (ADX) rats by means of the stopped-flow microperfusion technique and by measurement of tubular acidification kinetics with pH microelectrodes. Rats were adrenalectomized 48 h before experiments, and aldosterone, corticosterone and 18-OH corticosterone (18-OH-B) were given intramuscularly 100 and 40 min before starting the experiments. Stationary proximal luminal pH increased from 6.78 to 7.03 after ADX, while acidification half-times (t1/2) increased from 4.41 to 11.43 s. In consequence, net bicarbonate reabsorption fell from 2.18 to 0.50 nmol/cm2 X s after ADX. The administration of the three hormones stimulated tubular acidification, bicarbonate reabsorption reaching 1.18-1.28 nmol/cm2 X s. These data suggest that proximal tubular acidification is stimulated by both mineralo- and glucocorticoid hormones and by 18-OH-B; their mechanisms of action is discussed on the basis of a recently described model.
通过停流微灌注技术以及使用pH微电极测量肾小管酸化动力学,研究了皮质类固醇激素在对照、假手术和肾上腺切除(ADX)大鼠近端肾小管酸化中的作用。在实验前48小时对大鼠进行肾上腺切除,并在开始实验前100分钟和40分钟肌肉注射醛固酮、皮质酮和18-羟基皮质酮(18-OH-B)。肾上腺切除后,近端管腔稳定pH从6.78升至7.03,而酸化半衰期(t1/2)从4.41秒增加到11.43秒。因此,肾上腺切除后净碳酸氢盐重吸收从2.18降至0.50 nmol/cm2×秒。三种激素的给药刺激了肾小管酸化,碳酸氢盐重吸收达到1.18 - 1.28 nmol/cm2×秒。这些数据表明,近端肾小管酸化受到盐皮质激素、糖皮质激素以及18-OH-B的刺激;根据最近描述的模型讨论了它们的作用机制。