RENAL HANDLING OF PARATHYROID-HORMONE - ROLE OF PERITUBULAR UPTAKE AND GLOMERULAR-FILTRATION
RENAL HANDLING OF PARATHYROID-HORMONE - ROLE OF PERITUBULAR UPTAKE AND GLOMERULAR-FILTRATION
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DOI：
10.1172/jci108834
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发表时间：
1977-01-01
影响因子：
15.9
通讯作者：
SLATOPOLSKY, E
中科院分区：
文献类型：
--
作者：
MARTIN, KJ;HRUSKA, KA;SLATOPOLSKY, E
本文研究了麻醉犬输尿管结扎前后肾脏摄取甲状旁腺激素(PTH)的机制。持续输注牛甲状旁腺素(b-PTH 1-84)时，免疫反应性甲状旁腺素(i-PTH)的肾动静脉(A-V)差为22.+-。2%。输尿管结扎后，肾血流量无变化，A-V、I-PTH降至15.0±-。1%(P<；0.01)，表明肾小管周围持续显著摄取I-PTH，肾小球滤过(GF)在肾摄取I-PTH中的作用较小。由于在正常情况下，微量的甲状旁腺素出现在最终的尿液中，因此在KCN抑制肾小管重吸收之前和之后，在离体狗的灌流肾中，进一步研究了GF和随后的小管重吸收的贡献。每100mlGF的尿i-PTH由8.+-上升。4 ng/min(对照)至170.+-。氰化钾后45 ng/min。因此，甲状旁腺激素通常被肾小管上皮细胞过滤和重吸收。在建立输尿管结扎的情况下，通过单次注射b-PTH1-84或合成b-PTH1-34来研究这两种肾PTH摄取机制的生理作用。注射b-PTH1-84后，肾A-V I-PTH仅为20%，而有生物活性的完整PTH存在(15-20分钟)。肾小管周围未见甲状旁腺激素羧基末端摄取。相比之下，注射合成b-甲状旁腺素1-34后，输尿管结扎后肾组织N-末端i-甲状旁腺素抽出(13.4±-。0.6%对19.6.+-对照组为0.9%)，只要I-PTH在循环中持续。生长因子和肾小管周围摄取都是肾摄取PTH的重要机制。肾摄取甲状旁腺激素的羧基末端片段完全依赖于生长因子和肾小管的重吸收，而肾小管周围摄取只能在生物活性的b-甲状旁腺素1-84和合成的b-甲状旁腺素1-34中被证实。
The mechanisms of uptake of parathyroid hormone (PTH) by the kidney was studied in anesthetized dogs before and after ureteral ligation. During constant infusion of bovine PTH (b-PTH 1-84), the renal arteriovenous (A-V) difference for immunoreactive PTH (i-PTH) was 22 .+-. 2%. After ureteral ligation and no change in renal plasma flow, A-V i-PTH fell to 15 .+-. 1% (P < 0.01), indicating continued and significant uptake of i-PTH at peritubular sites and a lesser role of glomerular filtration (GF) in the renal uptake of i-PTH. Since, under normal conditions, minimal i-PTH appears in the final urine, the contribution of GF and subsequent tubular reabsorption was further examined in isolated perfused dog kidneys before and after inhibition of tubular reabsorption by KCN. Urinary i-PTH per 100 ml GF rose from 8 .+-. 4 ng/min (control) to 170 .+-. 45 ng/min after potassium cyanide. Thus, i-PTH is normally filtered and reabsorbed by the tubular cells. The physiological role of these 2 mechanisms of renal PTH uptake was examined by giving single injections of b-PTH 1-84 or synthetic b-PTH 1-34 in the presence of established ureteral ligation. After injection of b-PTH 1-84, renal A-V i-PTH was 20% only while biologically active intact PTH was present (15-20 min). No peritubular uptake of carboxyl terminal PTH fragments was demonstrable. In contrast, after injection of synthetic b-PTH 1-34, renal extraction of N-terminal i-PTH after ureteral ligation (which was 13.4 .+-. 0.6% vs. 19.6 .+-. 0.9% in controls) continued for as long as i-PTH persisted in the circulation. Both GF and peritubular uptake are important mechanisms for renal PTH uptake. Renal uptake of carboxyl terminal fragments of PTH is dependent exclusively upon GF and tubular reabsorption, whereas peritubular uptake can only be demonstrated for biologically active b-PTH 1-84 and synthetic b-PTH 1-34.