Role of extra- and intracellular calcium and calmodulin in renin release from rat kidney.
Role of extra- and intracellular calcium and calmodulin in renin release from rat kidney.
复制标题
DOI：
10.1210/endo-117-2-601
复制
发表时间：
1985-08
期刊：
影响因子：
4.8
通讯作者：
I. Antonipillai;Richard Horton
中科院分区：
文献类型：
--
作者：
I. Antonipillai;Richard Horton
肾小球细胞释放的肾素似乎与钙离子浓度呈负相关。我们研究了Ca+2的作用，以证实最近的研究结果，并进一步探讨细胞内钙以及钙-钙调素系统在肾素释放中的作用。使用大鼠肾皮质切片制备。异丙肾上腺素（10（-6）M）引起显著的肾素释放刺激，而血管紧张素（AII; 5 × 10（-5）M）抑制基础以及异丙肾上腺素刺激的肾素释放。从缓冲液中去除钙逆转了AII对肾素释放的抑制。硝苯地平（10（-5）M），一种特异性钙通道阻滞剂，诱导基础肾素释放显著增加。TMB-8是一种细胞内钙释放抑制剂，也引起基础肾素释放的剂量相关增加。钙调素拮抗剂三氟拉嗪和calmidazolium均引起显著的剂量相关性增加;然而，calmidazolium是一种更有效的刺激剂。低细胞外钙或硝苯地平浓度并不改变异丙肾上腺素诱导的肾素释放。在三氟拉嗪和钙咪达唑存在下，异丙肾上腺素进一步刺激肾素释放。这些结果表明，急性β-肾上腺素能刺激肾素不依赖于细胞外和细胞内钙和钙调素水平的变化。这些研究进一步证明，与大多数其他分泌系统不同，肾肾小球细胞中细胞内钙的减少或钙-钙调蛋白系统的抑制起促分泌剂的作用。
Renin release from the juxtaglomerular cell appears to be inversely related to calcium concentration. We studied the role of Ca+2 to confirm recent findings and to further explore the role of intracellular calcium as well as the calcium-calmodulin system in renin release. A rat renal cortical slice preparation was used. Isoproterenol (10(-6) M) caused significant stimulation of renin release, whereas angiotensin (AII; 5 X 10(-5) M) suppressed basal as well as isoproterenol-stimulated renin release. Removal of calcium from the buffer reversed AII suppression of renin release. Nifedipine (10(-5) M), a specific calcium channel blocker, induced a marked increase in basal renin release. TMB-8, an inhibitor of intracellular calcium release, also caused a dose-related increase in basal renin release. The calmodulin antagonists trifluoperazine and calmidazolium both caused significant dose-related increases; however, calmidazolium was a more potent stimulator. Low extracellular calcium or nifedipine concentrations did not alter isoproterenol-induced renin release. Isoproterenol further stimulated renin release in the presence of trifluoperazine and calmidazolium. These results suggest that acute beta-adrenergic stimulation of renin in independent of changes in levels of extracellular and intracellular calcium and calmodulin. These studies provide further evidence that unlike most other secretory systems, the reduction of intracellular calcium or inhibition of the calcium-calmodulin system in the juxtaglomerular cells of the kidney acts as a secretogogue.