蜂毒肽对大鼠肾皮质切片中肾素和前列腺素E2释放的影响。

Effect of melittin on renin and prostaglandin E2 release from rat renal cortical slices.

作者信息

Churchill P C, Rossi N F, Churchill M C, Ellis V R

机构信息

Department of Physiology and Internal Medicine, Wayne State University, School of Medicine, Detroit, MI 48201.

出版信息

J Physiol. 1990 Sep;428:233-41. doi: 10.1113/jphysiol.1990.sp018209.

DOI:10.1113/jphysiol.1990.sp018209

PMID:2231411

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1181644/

Abstract

The present experiments were designed to determine the effect of melittin on renin secretion. Melittin is a polypeptide component of bee venom which stimulates phospholipase A2 activity, thereby increasing arachidonic acid release and prostaglandin (PG) synthesis, and which inhibits protein kinase C activity. Either of these actions might be expected to stimulate renin secretion, since renin secretion is stimulated by arachidonic acid and by several PGs, and since renin secretion is inhibited by several activators of protein kinase C. 2. In rat renin cortical slices incubated at 37 degrees C in a buffered and oxygenated physiological saline solution, 0.1-10 microM-melittin produced a concentration-dependent stimulation of both prostaglandin E2 (PGE2) synthesis and renin secretion. However, melittin-stimulated renin secretion is independent of melittin-stimulated phospholipase A2 activity, arachidonic acid release, and PG synthesis, since 20 microM-quinacrine (a phospholipase A2 antagonist) and 50 microM-meclofenamate (a cyclooxygenase antagonist) antagonized basal and melittin-stimulated PGE2 synthesis but had no effects on basal or melittin-stimulated renin secretion. 3. Furthermore, melittin-stimulated renin secretion is not produced by inhibition of protein kinase C, since an activator of protein kinase C (12-O-tetradecanoylphorbol 13-acetate, TPA), enhanced rather than antagonized melittin-stimulated renin secretion. Ouabain partially antagonized, but did not completely block, melittin-stimulated renin secretion. 4. Thus, melittin-stimulated phospholipase A2 activity probably accounts for stimulated PGE2 production, but not for stimulated renin secretion. The mechanism of melittin-stimulated renin secretion is unclear; an effect on protein kinase C does not appear to be involved, and in contrast to the stimulatory effects of a variety of other substances, melittin-stimulated renin secretion is only partially antagonized by ouabain.

摘要

本实验旨在确定蜂毒肽对肾素分泌的影响。蜂毒肽是蜂毒的一种多肽成分，它能刺激磷脂酶A2的活性，从而增加花生四烯酸的释放和前列腺素（PG）的合成，并且能抑制蛋白激酶C的活性。这些作用中的任何一种都可能预期会刺激肾素分泌，因为花生四烯酸和几种前列腺素能刺激肾素分泌，而且几种蛋白激酶C的激活剂能抑制肾素分泌。2. 在37℃下于缓冲且充氧的生理盐溶液中孵育的大鼠肾皮质切片中，0.1 - 10微摩尔/升的蜂毒肽对前列腺素E2（PGE2）的合成和肾素分泌均产生浓度依赖性刺激作用。然而，蜂毒肽刺激的肾素分泌与蜂毒肽刺激的磷脂酶A2活性、花生四烯酸释放及PG合成无关，因为20微摩尔/升的奎纳克林（一种磷脂酶A2拮抗剂）和50微摩尔/升的甲氯芬那酸（一种环氧化酶拮抗剂）可拮抗基础状态及蜂毒肽刺激的PGE2合成，但对基础状态或蜂毒肽刺激的肾素分泌无影响。3. 此外，蜂毒肽刺激的肾素分泌并非由抑制蛋白激酶C产生，因为蛋白激酶C的激活剂（12 - O - 十四酰佛波醇13 - 乙酸酯，TPA）增强而非拮抗蜂毒肽刺激的肾素分泌。哇巴因部分拮抗但未完全阻断蜂毒肽刺激的肾素分泌。4. 因此，蜂毒肽刺激的磷脂酶A2活性可能是刺激PGE2产生的原因，但不是刺激肾素分泌的原因。蜂毒肽刺激肾素分泌的机制尚不清楚；似乎不涉及对蛋白激酶C的作用，并且与多种其他物质的刺激作用相反，蜂毒肽刺激的肾素分泌仅被哇巴因部分拮抗。