McLaughlin C W
J Physiol. 1984 Jan;346:419-37. doi: 10.1113/jphysiol.1984.sp015032.
The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa-positive voltage-clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non-transporting, amiloride-treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(-7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone-treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)
用林格氏钠溶液冲洗蟾蜍膀胱黏膜表面、用改良的莱博维茨组织培养基冲洗浆膜表面，所产生的二氧化碳通过对钠转运和时间进行多重回归分析。评估了与转运相关的代谢和基础代谢所贡献的比例，并确定了这些比例随时间变化的程度。这种提高了基底上代谢估计准确性的分析方法，被用于研究抗利尿激素、醛固酮和黏膜正向电压钳制对代谢的影响。抗利尿激素（0.05单位/毫升）平均使钠转运增加2.9倍，同时增加了这些转运组织中的二氧化碳产生速率，它还改变了用氨氯吡脒处理的非转运对照半膀胱的二氧化碳产生。对于每个半膀胱，将抗利尿激素作用后钠转运与基底上二氧化碳产生的比率与抗利尿激素作用前观察到的比率进行比较。当对成对的转运半膀胱的二氧化碳产生量校正抗利尿激素对基础二氧化碳产生的影响时，比率之间的差异大大减小。通过这种分析，证实抗利尿激素不会改变钠转运的化学计量。在抗利尿激素反应峰值附近施加30毫伏的黏膜正向电压钳制，进一步增加了钠转运和二氧化碳产生。在这些条件下，该组织的主动钠转运最大速率必定已接近，未观察到钠与基底上二氧化碳比率的改变。添加醛固酮（10⁻⁷摩尔）约4小时后，主动钠转运增加了一倍多。然而，相关的基底上二氧化碳产生增加超过了三倍。因此，虽然抗利尿激素和电压钳制引起的刺激对钠转运与基底上二氧化碳产生的比率没有影响，但该比率因醛固酮而显著降低。当通过电压钳制进一步增加醛固酮处理膀胱的钠转运时，钠转运与基底上二氧化碳产生的比率保持在降低的值。当醛固酮处理的半膀胱在抗利尿激素后进行电压钳制时，钠转运增加约35%以上，对照配对半膀胱仅暴露于抗利尿激素和电压钳制。（摘要截断于400字）
