Cortas N, Abras E, Arnaout M, Mooradian A, Muakasah S
J Clin Invest. 1984 Jan;73(1):46-52. doi: 10.1172/JCI111205.
Experiments were designed to determine whether the stimulatory effect of aldosterone on sodium transport involves an increase in tissue ATP. Urinary bladders that were removed from toads presoaked in 0.6% saline for 48-72 h, mounted as sacs, and maintained in open circuit except for brief observation of short circuit current every 30 min responded to 100 nM aldosterone added to the serosal bath with an increase in short circuit current to 170% of control hemibladders, which plateaus at 2-3 h. Tissue (ATP)/(ADP) X (Pi) measured in perchloric acid extracts increased to a maximum of 208% of controls (P less than 0.001) and ATP increased to 116% of controls (P less than 0.01) at 180 min. The short circuit current response to aldosterone paralleled the increase in ATP and (ATP)/(ADP) X (Pi) measured at 75, 120, 180, and 240 min. In bladders clamped at -150 mV, the short circuit current response to aldosterone was greater: 280% of controls (P less than 0.001) and tissue (ATP)/(ADP) X (Pi) increased to 191% of controls (P less than 0.001). In continuously short circuited bladders and bladders clamped at +75 mV, the short circuit current response to aldosterone and the change in ATP, ADP, or Pi were markedly diminished. 100 microM amiloride added to mucosal bath decreased the short circuit current to zero and inhibited the short circuit current response to aldosterone, whereas tissue ATP increased to 141% (P less than 0.05). 100, 250, and 500 microM NaCN dropped the short circuit current to 59, 35, and 24% of control values, respectively. Concurrently, tissue ATP measured at 60 min after the addition of NaCN dropped to 79, 66, and 56% of control values, respectively, and tissue ATP/ADP dropped to 68, 50, and 40%, respectively. The data revealed significant correlation between the change in the rate of sodium transport produced by aldosterone or NaCN as measured by the short circuit current and the concentration of ATP (r = 0.96, P less than 0.001), as well as ATP/ADP (r = 0.95, P less than 0.001). In conclusion, these results support the view that the stimulatory effects of aldosterone on sodium transport involve an increase in ATP or (ATP)/(ADP) X (Pi).
设计实验以确定醛固酮对钠转运的刺激作用是否涉及组织三磷酸腺苷（ATP）的增加。将蟾蜍的膀胱取出，预先在0.6%盐水中浸泡48 - 72小时，制成囊袋并安装，除了每30分钟短暂观察短路电流外保持开路状态，向浆膜浴中添加100 nM醛固酮后，短路电流增加至对照半膀胱的170%，并在2 - 3小时达到平稳状态。用高氯酸提取物测量的组织（ATP）/（ADP）×（Pi）在180分钟时增加至对照的最大值208%（P小于0.001），ATP增加至对照的116%（P小于0.01）。醛固酮引起的短路电流反应与在75、120、180和240分钟测量的ATP以及（ATP）/（ADP）×（Pi）的增加平行。在钳制在 - 150 mV的膀胱中，醛固酮引起的短路电流反应更大：为对照的280%（P小于0.001），组织（ATP）/（ADP）×（Pi）增加至对照的191%（P小于0.001）。在持续短路的膀胱和钳制在 + 75 mV的膀胱中，醛固酮引起的短路电流反应以及ATP、二磷酸腺苷（ADP）或磷酸（Pi）的变化明显减弱。向黏膜浴中添加100 μM氨氯吡脒可使短路电流降至零，并抑制醛固酮引起的短路电流反应，而组织ATP增加至141%（P小于0.05）。100、250和500 μM的氰化钠（NaCN）分别使短路电流降至对照值的59%、35%和24%。同时，添加NaCN后60分钟测量的组织ATP分别降至对照值的79%、66%和56%，组织ATP/ADP分别降至68%、50%和40%。数据显示，通过短路电流测量的醛固酮或NaCN产生的钠转运速率变化与ATP浓度（r = 0.96，P小于0.001）以及ATP/ADP（r = 0.95，P小于0.001）之间存在显著相关性。总之，这些结果支持这样的观点，即醛固酮对钠转运的刺激作用涉及ATP或（ATP）/（ADP）×（Pi）增加。
