Van Dongen R, Peart W S
Br J Pharmacol. 1974 Jan;50(1):125-9. doi: 10.1111/j.1476-5381.1974.tb09599.x.
1 The effect of calcium on the inhibition of renin secretion by biologically active angiotensin was investigated in the isolated rat kidney perfused with Krebs-Ringer saline.2 In the presence of calcium (3.7 mM), asp(NH(2))'-angiotensin II suppressed both basal and isoprenaline-stimulated renin secretion. Renal perfusion pressure, which was increased by the infusion of angiotensin, returned to control levels when isoprenaline was added.3 When the calcium concentration was reduced to 0.32 mM, the vasoconstriction produced by angiotensin was abolished although the inhibitory effect on renin secretion was still evident.4 In the absence of calcium, angiotensin no longer suppressed basal renin secretion and a prompt increase in renin secretion occurred when isoprenaline was added.5 The higher basal renin levels which were observed in calcium-free perfusions, suggest the existence of an intrarenal calcium-dependent mechanism that regulates basal renin secretion.6 These observations indicate that the inhibitory effect of biologically active angiotensin, on basal and isoprenaline-stimulated renin secretion, is functionally related to the contractor response by its dependence on calcium. The recognition that the renin-producing cells are modified smooth muscle cells supports this association
在灌注了 Krebs-Ringer 生理盐水的离体大鼠肾脏中，研究了钙对生物活性血管紧张素抑制肾素分泌的影响。
在存在钙（3.7 mM）的情况下，天冬氨酰（NH₂）-血管紧张素 II 抑制基础和异丙肾上腺素刺激的肾素分泌。因输注血管紧张素而升高的肾灌注压，在加入异丙肾上腺素后恢复到对照水平。
当钙浓度降至 0.32 mM 时，血管紧张素产生的血管收缩作用消失，尽管对肾素分泌的抑制作用仍然明显。
在无钙情况下，血管紧张素不再抑制基础肾素分泌，加入异丙肾上腺素后肾素分泌迅速增加。
在无钙灌注中观察到的较高基础肾素水平，提示存在一种调节基础肾素分泌的肾内钙依赖性机制。
这些观察结果表明，生物活性血管紧张素对基础和异丙肾上腺素刺激的肾素分泌的抑制作用，在功能上与其对钙的依赖性收缩反应相关。认识到产生肾素的细胞是修饰的平滑肌细胞支持了这种关联。
