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培养的大鼠髓质内集合管细胞中前列腺素E2合成的调控:钙的作用

Control of prostaglandin E2 synthesis in cultured rat inner medullary collecting tubule cells: the role of calcium.

作者信息

Teitelbaum I, Wolf A, Berl T

出版信息

Miner Electrolyte Metab. 1986;12(5-6):308-13.

PMID:3100918
Abstract

We investigated the role of calcium in basal, ionophore- and hormone-stimulated prostaglandin E2 (PGE2) production by rat inner medullary collecting tubule cells. Basal PGE2 production is significantly decreased in the absence of calcium (4.49 +/- 0.79 vs. 19.99 +/- 3.47 pg/micrograms protein/h, p less than 0.001). No further increment is seen at 4 mM calcium. The ability of the calcium ionophore A23187 to stimulate PG production is proportional to the amount of calcium present in the extracellular space. Bradykinin is a potent stimulus to PG production even in the virtual absence of calcium while arginine vasopressin has only a modest effect. Neither bradykinin nor arginine vasopressin exhibit any further PG stimulation at 1 mM calcium; both bradykinin and arginine vasopressin increase PGE2 production significantly when calcium is increased to a supraphysiologic level. The data suggests an important role for intracellular rather than extracellular calcium in the control of PG production. Bradykinin but not vasopressin display significant calcium-independent stimulatory effects on PG synthesis.

摘要

我们研究了钙在大鼠髓质内集合管细胞基础状态、离子载体及激素刺激下前列腺素E2(PGE2)生成过程中的作用。在无钙情况下,基础PGE2生成显著减少(4.49±0.79 vs. 19.99±3.47 pg/μg蛋白质/小时,p<0.001)。在4 mM钙时未见进一步增加。钙离子载体A23187刺激PG生成的能力与细胞外空间中存在的钙量成正比。即使在几乎无钙的情况下,缓激肽仍是PG生成的有效刺激物,而精氨酸加压素只有适度作用。在1 mM钙时,缓激肽和精氨酸加压素均未表现出任何进一步的PG刺激作用;当钙增加到超生理水平时,缓激肽和精氨酸加压素均显著增加PGE2生成。数据表明,细胞内而非细胞外钙在PG生成的控制中起重要作用。缓激肽而非加压素对PG合成显示出显著的非钙依赖性刺激作用。

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