Schryver S, Sanders E, Beierwaltes W H, Romero J C
Kidney Int. 1984 Mar;25(3):512-8. doi: 10.1038/ki.1984.47.
This study was performed (1) to evaluate the ability of renal superficial (SP) and juxtamedullary (JM) isolated glomeruli to synthesize 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and prostaglandin E2 (PGE2) when stimulated with different doses of arachidonic acid (AA) and (2) to determine the differential effects that the formation of these prostaglandins may have on renin release. Renal SP and JM glomeruli were isolated separately from dog renal cortex using a passive sieving technique. Glomeruli were superfused within glass chambers with a Krebs Ringer solution and three different concentrations of AA. Effluent concentrations of 6-keto-PGF1 alpha (primary metabolite of PGI2), PGE2, and renin were determined by radioimmunoassay. Synthesis of 6-keto-PGF1 alpha by SP glomeruli increased in a dose-dependent manner in response to the three increasing concentrations of AA. These three doses of AA also evoked proportional increments in the release of renin which were significantly correlated with the increases in 6-keto-PGF1 alpha. In contrast, PGE2 synthesis was maximally stimulated by all doses of AA and was not correlated with renin release. In JM glomeruli, AA evoked the same pattern in the synthesis of 6-keto-PGF1 alpha and PGE2. However, renin release increased significantly only with the perfusion of the highest concentration of AA. These perfusion results show that SP and JM glomeruli have the same ability to synthesize 6-keto-PGF1 alpha and PGE2. However, renin release was significantly higher in SP than in JM glomeruli and correlated with 6-keto-PGF1 alpha synthesis.
(1)评估肾浅表(SP)和近髓(JM)分离肾小球在不同剂量花生四烯酸(AA)刺激下合成6-酮-前列腺素F1α(6-酮-PGF1α)和前列腺素E2(PGE2)的能力;(2)确定这些前列腺素的形成对肾素释放可能产生的差异效应。采用被动筛分技术从犬肾皮质中分别分离出肾SP和JM肾小球。将肾小球置于玻璃小室中,用 Krebs-Ringer 溶液和三种不同浓度的 AA 进行灌流。通过放射免疫分析法测定流出液中6-酮-PGF1α(前列环素I2的主要代谢产物)、PGE2和肾素的浓度。随着三种AA浓度的增加,SP肾小球合成6-酮-PGF1α呈剂量依赖性增加。这三种剂量的AA也引起肾素释放成比例增加,且与6-酮-PGF1α的增加显著相关。相反,所有剂量的AA均最大程度刺激PGE2合成,且与肾素释放无关。在JM肾小球中,AA引起6-酮-PGF1α和PGE2合成的相同模式。然而,仅在灌注最高浓度AA时肾素释放才显著增加。这些灌流结果表明,SP和JM肾小球具有相同的合成6-酮-PGF1α和PGE2的能力。然而,SP肾小球中的肾素释放显著高于JM肾小球,且与6-酮-PGF1α合成相关。