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The urinary system consists of two kidneys, two ureters, the urinary bladder, and the urethra.
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The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
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Related Experiment Video

Updated: May 6, 2026

Epithelial Cell Repopulation and Preparation of Rodent Extracellular Matrix Scaffolds for Renal Tissue Development
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Pericytes synthesize renin.

Alison C Berg1, Catalina Chernavvsky-Sequeira, Jennifer Lindsey

  • 1Alison C Berg, Catalina Chernavvsky-Sequeira, Jennifer Lindsey, R Ariel Gomez, Maria Luisa S Sequeira-Lopez, Department of Pediatrics, University of Virginia School of Medicine, Charlottesville, VA 22908, United States.

World Journal of Nephrology
|November 1, 2013
PubMed
Summary
This summary is machine-generated.

Kidney pericytes produce renin during development. In mice lacking angiotensinogen (AGT), renin-expressing pericytes significantly increase, indicating a response to this early-life homeostatic challenge.

Keywords:
Angiotensin deficiencyAngiotensinogenDevelopmentGene deletionHomeostasisInterstitiumKidneyRenin angiotensin system

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Area of Science:

  • Nephrology
  • Developmental Biology
  • Renal Physiology

Background:

  • Pericytes are crucial cells in kidney development and function.
  • Renin is a key enzyme in the renin-angiotensin-aldosterone system (RAAS).
  • The role of pericytes in renin production during development is not fully understood.

Purpose of the Study:

  • To investigate renin expression in kidney pericytes during normal development.
  • To determine how the absence of angiotensinogen (AGT) affects renin expression in pericytes.

Main Methods:

  • Immunohistochemistry was used to identify renin-expressing cells in wild-type (WT) and AGT-deficient (AGT -/-) mice.
  • Analysis was performed at various developmental stages from embryonic day 18 to postnatal day 70.
  • The density of renin-positive pericytes was quantified and compared between WT and AGT -/- groups.

Main Results:

  • In WT mice, renin-positive pericyte density was stable from fetal life until weaning and decreased significantly in adulthood.
  • AGT -/- mice showed no significant difference in renin-positive pericyte density at E18 and P1 compared to WT.
  • However, AGT -/- mice exhibited a marked and sustained increase in renin-positive pericytes from P5 onwards, peaking at P10.

Conclusions:

  • Interstitial pericytes are a source of renin during kidney development.
  • The absence of angiotensinogen triggers a significant increase in renin-expressing pericytes, suggesting a compensatory mechanism.
  • This highlights the adaptability of pericytes in response to early-life homeostatic challenges.