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肿瘤性合成甲状旁腺激素相关肽抑制培养的肾上皮细胞中氨氯地平敏感的钠转运。

Tumoral synthetic parathyroid hormone related peptide inhibits amiloride-sensitive sodium transport in cultured renal epithelia.

作者信息

Caverzasio J, Rizzoli R, Martin T J, Bonjour J P

机构信息

Department of Medicine, University Hospital, Geneva, Switzerland.

出版信息

Pflugers Arch. 1988 Nov;413(1):96-8. doi: 10.1007/BF00581235.

Abstract

The amino-terminal fragment of a tumor parathyroid hormone-related peptide (PTHrP(1-34] produced by a human squamous cell carcinoma of the lung was recently synthesized. In the present work its effect on the amiloride-sensitive sodium transport, taken as an estimate of the Na+/H+ exchanger activity of cultured opossum kidney (OK) epithelia was compared to that of synthetic bovine parathyroid hormone (bPTH(1-34]. Both PTHrP(1-34) and bPTH(1-34) inhibited the initial rate of amiloride-sensitive 22Na transport. Half maximal inhibitory activity was obtained at about 10(-11)M for both PTHrP(1-34) and bPTH(1-34). In conclusion, tumoral PTHrP(1-34) appears to be as effective as bPTH(1-34) for inhibiting the amiloride-sensitive Na transport, and presumably for decreasing the activity of the Na+/H+ exchanger present in the apical membrane of kidney epithelial cells.

摘要

人肺鳞状细胞癌产生的肿瘤甲状旁腺激素相关肽(PTHrP(1-34))的氨基末端片段最近已被合成。在本研究中,将其对氨氯地平敏感的钠转运的影响(以此作为培养的负鼠肾(OK)上皮细胞Na+/H+交换活性的估计)与合成牛甲状旁腺激素(bPTH(1-34))的影响进行了比较。PTHrP(1-34)和bPTH(1-34)均抑制氨氯地平敏感的22Na转运的初始速率。PTHrP(1-34)和bPTH(1-34)在约10(-11)M时均获得半数最大抑制活性。总之,肿瘤性PTHrP(1-34)在抑制氨氯地平敏感的钠转运方面似乎与bPTH(1-34)一样有效,并且推测在降低肾上皮细胞顶端膜中存在的Na+/H+交换器的活性方面也是如此。

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