ROLE OF C-AMP IN RENIN RELEASE

体内研究表明，肾素的释放受三个因素控制 肾内机制--压力感受器、致密黄斑和 β-肾上腺素受体。许多证据支持这样一种观点 前列腺素I2作为细胞外介质连接血管内皮细胞活化 肾小球旁细胞释放肾素的压力感受器或致密斑区。 类似地，去甲肾上腺素作为细胞外介质连接 肾小球旁激活β受体对肾素释放的影响 细胞。因为前列腺素I2和β肾上腺素受体激动剂都可以 刺激肾小球旁细胞释放肾素，由于腺苷是 抑制作用，我们认为环磷酸腺苷作为一种 细胞内介质。 肾素刺激或抑制肾素的多种物质的使用 和肾小球旁细胞环磷酸腺苷的产生(例如。 前列腺素I2，异丙肾上腺素，9-取代腺苷衍生物， 磷酸二酯酶抑制剂、蛋白激酶抑制剂)将用于 检验我们的假设。肾素释放和环腺苷的研究数据 用细胞放射免疫测定法测定单磷酸盐的产生 将对富含肾小球旁细胞的培养系统进行评估。

In vivo studies indicate that renin release is controlled by three intrarenal mechanisms-the baroreceptor, macula densa and beta-adrenoreceptors. Much evidence supports the concept that prostaglandin I2 serves as extracellular mediator linking activation of baroreceptor or macula densa to renin release by juxtaglomerular cells. Similarly, norepinephrine serves as extracellular mediator linking activation of beta adrenoreceptor to renin release by juxtaglomerular cells. Since both prostaglandin I2 and beta adrenoreceptor agonists can stimulate release of renin by juxtaglomerular cells, and since adenosine is inhibitory, we propose that cyclic adenosine monophosphate serves as the intracellular mediator. The use of a number of substances which either stimulate or inhibit renin and cyclic adenosine monophosphate production in juxtaglomerular cells (eg. prostaglandin I2, isoproterenol, 9-substituted adenosine derivatives, phosphodiesterase inhibitors, protein kinase inhibitors) will be used to test our hypothesis. Data on renin release and cyclic adenosine monophosphate production as determined by radioimmunoassay on a cell culture system enriched in juxtaglomerular cells will be evaluated.