Interaction of the prostaglandin and renin-angiotensin systems in isolated rat glomeruli.
Interaction of the prostaglandin and renin-angiotensin systems in isolated rat glomeruli.
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离体大鼠肾小球中前列腺素和肾素-血管紧张素系统的相互作用。
DOI：
10.1152/ajprenal.1980.239.6.f602
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Romero,JC
中科院分区：
文献类型：
--
作者：
Beierwaltes,WH;Schryver,S;Olson,PS;Romero,JC
使用被动机械筛分技术从大鼠肾脏分离肾小球。将40-50 mg肾小球的悬浮液置于玻璃室中，并用改良的Krebs-Ringer溶液灌注。使用放射免疫测定法测定10分钟馏分的流出物收集的肾素或前列腺素（PG）E2浓度。改变灌注液，使其含有β-肾上腺素能激动剂异丙肾上腺素、血管紧张素II或花生四烯酸。1.78或8.1 × 10 ~（-4）M的异丙肾上腺素可使肾素显著释放，但PGE ~ 2浓度不受影响。异丙肾上腺素刺激的肾素释放被1.2 × 10（-4）M普萘洛尔阻断，但不受6.3 × 10（-6）M甲氨蝶呤的影响。4或40 × 10（-9）M的血管紧张素II既不改变肾素也不改变PGE 2。给予1.6或16.0 × 10（-5）M花生四烯酸可使PG合成显著增加，并刺激肾素的显著释放。用6.3 × 10（-6）M的甲氨蝶呤处理肾小球可减少PGE 2的合成并抑制肾素的释放，但1.2 × 10（-4）M的普萘洛尔对PG的合成和同时的肾素释放没有影响。这些结果提供了直接的证据之间的相互关联的机制，肾肾上腺素和肾素释放是独立的外部管或血液动力学刺激，并表明，β-肾上腺素途径的肾素刺激是独立的任何修改的影响所施加的肾上腺素。
Renal glomeruli were isolated from rat kidneys using a passive mechanical sieving technique. Suspensions of 40–50 mg glomeruli were placed in glass chambers and superfused by a modified Krebs-Ringer solution. Effluent collections of 10-min fractions were measured for renin or prostaglandin (PG) E2 concentration using radioimmunoassays. The perfusate was altered to contain either the beta-adrenergic agonist isoproterenol, angiotensin II, or arachidonic acid. Isoproterenol at 1.78 or 8.1 X 10(-4) M produced a significant release of renin, but the concentration of PGE2 was unaffected. Isoproterenol-stimulated renin release was blocked by 1.2 X 10(-4) M propranolol but was unaffected by 6.3 X 10(-6) M meclofenamate. Angiotensin II at 4 or 40 X 10(-9) M altered neither renin nor PGE2. Arachidonic acid administered at 1.6 or 16.0 X 10(-5) M produced a marked increase in PG synthesis and stimulated a significant release of renin. Treatment of glomeruli with 6.3 X 10(-6) M meclofenamate attenuated PGE2 synthesis and abolished renin release, but 1.2 X 10(-4) M propranolol had no effect on PG synthesis or the coincident release of renin. These results give direct evidence of an interrelating mechanism between renal prostaglandins and renin release that is independent of external tubular or hemodynamic stimuli and show that the beta-adrenergic pathway of renin stimulation is independent of any modifying influence exerted by prostaglandins.