Renin is stored in juxtaglomerular cells within granules and is thought to be released by exocytosis. The release of renin is precisely regulated by intracellular signal cascades, which either stimulate or inhibit renin secretion. The cyclic AMP pathway involving activation of protein kinase A potently stimulates renin secretion. The efficacy of the cAMP pathway is firstly determined by the balance of factors stimulating (example: ?-adrenoreceptor) or inhibiting adenylate cyclase (example: adenosine A1 receptor) as well as by the activity of cAMP-phosphodiesterases (PDE-3, PDE-4). Secondly, the efficacy of the stimulatory cAMP pathway is controlled by an inhibitory calcium dependent signaling route, which is powerful enough to virtually blunt any stimulation of renin secretion by cAMP. This inhibitory pathway is for example initiated by angiotensin II or by endothelins and their effects require both intracellular calcium release as well as transmembrane calcium influx. Further downstream elements of the inhibitory calcium dependent pathway are still subject of speculation. The same holds for the mechanism of the inhibitory effect of protein kinase G (type II) on renin secretion from juxtaglomerular cells. The final mechanisms that control the fusion of renin containing vesicles with the plasma membrane during the event of exocytosis are yet also only poorly understood.