Pflügers Archiv - European Journal of Physiology

, Volume 465, Issue 1, pp 59–69

The influence of extracellular and intracellular calcium on the secretion of renin

Invited Review

DOI: 10.1007/s00424-012-1107-x

Cite this article as:
Atchison, D.K. & Beierwaltes, W.H. Pflugers Arch - Eur J Physiol (2013) 465: 59. doi:10.1007/s00424-012-1107-x


Changes in plasma, extracellular, and intracellular calcium can affect renin secretion from the renal juxtaglomerular (JG) cells. Elevated intracellular calcium directly inhibits renin release from JG cells by decreasing the dominant second messenger intracellular cyclic adenosine monophosphate (cAMP) via actions on calcium-inhibitable adenylyl cyclases and calcium-activated phosphodiesterases. Increased extracellular calcium also directly inhibits renin release by stimulating the calcium-sensing receptor (CaSR) on JG cells, resulting in parallel changes in the intracellular environment and decreasing intracellular cAMP. In vivo, acutely elevated plasma calcium inhibits plasma renin activity (PRA) via parathyroid hormone-mediated elevations in renal cortical interstitial calcium that stimulate the JG cell CaSR. However, chronically elevated plasma calcium or CaSR activation may actually stimulate PRA. This elevation in PRA may be a compensatory mechanism resulting from calcium-mediated polyuria. Thus, changing the extracellular calcium in vitro or in vivo results in inversely related acute changes in cAMP, and therefore renin release, but chronic changes in calcium may result in more complex interactions dependent upon the duration of changes and the integration of the body’s response to these changes.


Calcium-sensing receptor Hypercalcemia Parathyroid hormone cAMP Juxtaglomerular cell Adenylyl cyclase 

Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  • Douglas K. Atchison
    • 1
    • 2
  • William H. Beierwaltes
    • 1
    • 2
  1. 1.Hypertension and Vascular Research Division, Department Internal MedicineHenry Ford HospitalDetroitUSA
  2. 2.Department of PhysiologyWayne State University School of MedicineDetroitUSA

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