Fray J C, Lush D J, Valentine A N
Fed Proc. 1983 Dec;42(15):3150-4.
Renin secretion from the juxtaglomerular cell is controlled by numerous receptors, humoral agents, and ions. Recently, a stretch receptor hypothesis has been advanced to suggest that all of these diverse factors control renin secretion by a mechanism initiated by a fall in cytoplasmic Ca2+. This fall in Ca2+ may be achieved by lowering Ca2+ influx, raising Ca2+ efflux, or sequestering Ca2+ into cellular organelles and binding sites. The increased renin secretion observed with low arterial pressure, beta-adrenergic agonists, parathyroid hormone, glucagon, cyclic AMP, prostaglandins, low Ca2+ and Ca2+ ionophore, high Mg2+, and Na+ and Cl- may be explained in this context. On the other hand, the decreased renin secretion observed with high pressure, alpha-adrenergic agonists, some prostaglandins, angiotensin, vasopressin, and high K+ may be explained by a rise in cytoplasmic Ca2+ mediated by an opposite sequence of events. Recent observations suggest that the fall in cytoplasmic Ca2+ sets in motion the transport of renin from its site of storage (granules) or synthesis into the cytoplasmic space and finally across the plasma membrane. Thus although renin is stored in granules, its secretion occurs by a process quite different from exocytosis.
肾小球旁细胞的肾素分泌受多种受体、体液因子和离子的控制。最近，一种牵张受体假说被提出，认为所有这些不同的因素都是通过细胞质Ca2+浓度下降引发的机制来控制肾素分泌的。Ca2+浓度的下降可以通过降低Ca2+内流、增加Ca2+外流或把Ca2+隔离到细胞器和结合位点来实现。在低动脉压、β-肾上腺素能激动剂、甲状旁腺激素、胰高血糖素、环磷酸腺苷、前列腺素、低Ca2+和Ca2+离子载体、高Mg2+以及Na+和Cl-情况下观察到的肾素分泌增加，都可以在这种背景下得到解释。另一方面，在高压力、α-肾上腺素能激动剂、某些前列腺素、血管紧张素、血管升压素和高K+情况下观察到的肾素分泌减少，可能是由相反事件序列介导的细胞质Ca2+浓度升高所解释的。最近的观察表明，细胞质Ca2+浓度的下降启动了肾素从其储存部位（颗粒）或合成部位转运到细胞质空间并最终穿过质膜的过程。因此，尽管肾素储存在颗粒中，但其分泌过程与胞吐作用截然不同。
