Mode of action of parathyroid hormone and cyclic adenosine 3',5'-monophosphate on renal tubular phosphate reabsorption in the dog.
Mode of action of parathyroid hormone and cyclic adenosine 3',5'-monophosphate on renal tubular phosphate reabsorption in the dog.
复制标题
甲状旁腺激素和环腺苷 3,5-单磷酸对狗肾小管磷酸盐重吸收的作用方式。
DOI：
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发表时间：
1971
影响因子：
15.9
通讯作者：
M. Goldberg
中科院分区：
文献类型：
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作者：
Z. Agus;J. Puschett;D. Senesky;M. Goldberg
为了评价甲状旁腺激素和环磷酸腺苷对近端肾小管钠磷重吸收的影响，对接受高纯度甲状旁腺激素(PTH)、环状3‘，5’-腺苷一磷酸(CAMP)、5‘-AMP和生理盐水制剂的犬进行了显微穿刺术。甲状旁腺激素可抑制近端肾小管对钠和磷酸盐的重吸收，与全肾或单肾单位肾小球滤过率(GFR)升高无关。大部分近端排出的磷酸盐在最终尿液中排出，而钠的排泄轻微上升，尽管近端有明显的抑制，这与远端肾单位存在钠而不是磷酸盐的重吸收部位是一致的。在全肾或单个肾单位GFR均无改变的情况下，系统地或直接将二丁酰环AMP注入肾动脉可抑制近端钠和磷的重吸收，其作用在数量和质量上与甲状旁腺素相似。相反，另一种腺嘌呤核苷酸5‘-AMP不抑制钠或磷的重吸收。这些观察结果支持甲状旁腺素的肾脏效应是通过刺激肾皮质腺苷环化酶来实现的。中等剂量的生理盐水输注，25ml/kg，对近端肾小管部分钠和磷的重吸收也有类似的抑制作用，并伴有明显的磷酸盐尿，但仅有极少量的钠尿。因此，当钠的重吸收被抑制时，钠和磷的重吸收的变化在近端小管中平行地发生，无论是体积扩大还是给予特定的磷酸制剂，如甲状旁腺素或环磷酸腺苷。这些数据与磷酸盐重吸收依赖于近端肾小管钠重吸收的观点是一致的，其中甲状旁腺素的磷酸尿化作用可能是腺苷环化酶对近端肾小管钠重吸收的主要抑制作用的结果。
To evaluate the effects of parathyroid hormone and cyclic adenosine monophosphate on proximal tubular sodium and phosphate reabsorption, micropuncture studies were performed on dogs that received a highly purified preparation of parathyroid hormone (PTH), dibutyryl cyclic 3',5'-adenosine monophosphate (cyclic AMP), 5'-AMP, and saline. PTH resulted in a 30-40% inhibition of sodium and phosphate reabsorption in the proximal tubule unassociated with a rise in either total kidney or single nephron glomerular filtration rate (GFR). The bulk of the phosphate rejected proximally was excreted in the final urine while sodium excretion rose minimally despite the marked proximal inhibition, consistent with the presence of reabsorptive sites in the distal nephron for sodium but not phosphate. The infusion of dibutyryl cyclic AMP either systemically or directly into the renal artery inhibited proximal sodium and phosphate reabsorption in the absence of changes in either total kidney or single nephron GFR, resembling the effects of PTH quantitatively and qualitatively. In contrast, another adenine nucleotide, 5'-AMP, did not inhibit the reabsorption of either sodium or phosphate. These observations support the thesis that renal effects of PTH are mediated via stimulation of renal cortical adenyl cyclase. The infusion of a moderate saline load, 25 ml/kg, also produced a similar inhibition of proximal tubular fractional sodium and phosphate reabsorption with a marked phosphaturia but only minimal natriuresis. Thus, changes in sodium and phosphate reabsorption occur in parallel in the proximal tubule when sodium reabsorption is inhibited either with volume expansion or with administration of "specific" phosphaturic agents such as PTH or cyclic AMP. These data are consistent with the thesis that phosphate reabsorption is dependent upon proximal tubular sodium reabsorption wherein the phosphaturic effect of PTH might be the result of a primary inhibition of proximal tubular sodium reabsorption mediated by adenyl cyclase stimulation.