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花生四烯酸和前列腺素可增强钾刺激的钙流入大鼠脑突触体。

Arachidonic acid and prostaglandins enhance potassium-stimulated calcium influx into rat brain synaptosomes.

作者信息

Kandasamy S B, Hunt W A

机构信息

Behavioral Sciences Department, Armed Forces Radiobiology Research Institute, Bethesda, Maryland 20814-5145.

出版信息

Neuropharmacology. 1990 Sep;29(9):825-9. doi: 10.1016/0028-3908(90)90156-l.

Abstract

Exogenous administration of arachidonic acid, prostaglandins PGF2 alpha, PGD2 and PGE2 increased potassium-stimulated uptake of calcium in rat brain synaptosomes from the brain of the rat, but had no effect on the basal uptake of calcium. Arachidonic acid-induced uptake of calcium was mediated by its prostaglandin metabolites, because a cyclooxygenase inhibitor, indomethacin, inhibited the response. L-Type calcium channel blockers, such as verapamil, diltiazem and nimodipine, blocked both KCl- and prostaglandin-enhanced potassium-stimulated influx of calcium in the brain. These results suggest that prostaglandins act as a calcium ionophore, through L-type voltage-sensitive calcium channels.

摘要

外源性给予花生四烯酸、前列腺素PGF2α、PGD2和PGE2可增加大鼠脑突触体中钾刺激的钙摄取,但对钙的基础摄取无影响。花生四烯酸诱导的钙摄取是由其前列腺素代谢产物介导的,因为环氧化酶抑制剂吲哚美辛可抑制该反应。L型钙通道阻滞剂,如维拉帕米、地尔硫䓬和尼莫地平,可阻断氯化钾和前列腺素增强的脑内钾刺激的钙内流。这些结果表明,前列腺素通过L型电压敏感性钙通道作为钙离子载体发挥作用。

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