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Metabolic control of renin secretion

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Abstract

One emerging topic in renin–angiotensin system (RAS) research is the direct local control of renin synthesis and release by endogenous metabolic intermediates. 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 RAS activation in diabetes. GPR91 (also called SUCNR1) binds 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, succinate signaling via GPR91 appears to be an important mediator or modulator of renin secretion. This review summarizes our current knowledge on the control of renin release by molecules of endogenous metabolic pathways with the main focus on succinate/GPR91.

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Acknowledgments

This work was supported by DK64324 and the 1-11-BS-121 grant from the American Diabetes Association to J.P.P.

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Correspondence to János Peti-Peterdi.

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This article is published as part of the special issue on the Renin-Angiotensin System.

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Peti-Peterdi, J., Gevorgyan, H., Lam, L. et al. Metabolic control of renin secretion. Pflugers Arch - Eur J Physiol 465, 53–58 (2013). https://doi.org/10.1007/s00424-012-1130-y

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  • DOI: https://doi.org/10.1007/s00424-012-1130-y

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