SUMMARY Renin is a central hormone in the control of blood pressure and various other physiological functions. In spite of the very early discovery of renin over 100 years ago, we have only recently gained a deeper understanding of the origin of renin producing cells and of the mechanisms responsible for renin synthesis and secretion. The main source of renin is the juxtaglomerular cells (JGC), which release renin from storage granules. Besides the renin-angiotensin-system (RAS) in the JGC, there exist local RAS in various tissues. JGC originate in situ within the metanephric kidney from mesenchymal cells that are not related to smooth muscle lineages, as hitherto assumed. The previous notion that JGC stem from vascular smooth muscle cells may be explained by JGC differentiation: they acquire smooth muscle markers that are maintained throughout adulthood. It has become clear, that increasing intracellular free Ca2+ inhibits renin secretion in JGC. In contrast, cAMP stimulates renin release. Over the last decade, numerous studies obtained on isolated JGC and intact animals provided contradicting results as to whether cGMP has a stimulatory or inhibitory action on renin release. Newer results strongly suggest that cGMP effects on renin release from JGC involve the degradation of cAMP, which is modulated by cGMP. Finally, it has been found that the production of renin is not only modulated by enhancing or attenuating renin transcription, but that renin mRNA stability is controlled by various proteins present in renin producing cells.