The renin-angiotensin system (RAS) plays an important role in the physiological control of body fluid and electrolyte homeostasis and blood pressure maintenance. The mechanisms and importance of local, intra-renal, intra-tubular RAS components, and their direct local control by endogenous metabolic intermediates are emerging research topics in the field. During the past few years our laboratory has characterized the localization and signaling of the novel metabolic receptor GPR91 in the normal and diabetic kidney and established GPR91 as a new, direct link between high glucose and renin synthesis and release, the rate limiting steps in RAS activation especially in diabetes. GPR91 (also called SUCNR1) binds the tricarboxylic acid (TCA)-cycle intermediate succinate, which can rapidly accumulate in the local tissue environment when energy supply and demand are out of balance. In a variety of physiological and pathological conditions associated with metabolic stress, the classic mitochondrial intermediate succinate has a non-traditional signaling role via GPR91 which appears to be an important mediator or modulator of renin secretion. At the classic vascular anatomical site of renin synthesis in the juxtaglomerular apparatus (JGA), macula densa cells may sense succinate in the tubular fluid that is derived from cells of the proximal tubule or the thick ascending limb, and via luminal GPR91 receptors trigger renin release in a paracrine fashion. In addition to the JGA, renin and its precursor prorenin are also produced and released within the kidney at a new tubular site, in the renal collecting duct. Interestingly, renal GPR91 expression is the highest in the collecting duct, where succinate also appears to participate in the control of the local intra-tubular RAS via tubular cell-to-cell crosstalk. This lecture will summarize our current knowledge on the control of JGA and tubular renin release by succinate/GPR91.