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Published on: January 15, 2010
Renal dopaminergic defect in C57Bl/6J mice
Crisanto S Escano1, Ines Armando, Xiaoyan Wang
1Children's National Medical Center, Center for Molecular Physiology Research, Department of Pediatrics, George Washington School of Medicine and Health Sciences, Washington, DC, USA.
Summary
Defective kidney dopamine D(1)-like receptor function causes salt sensitivity in C57Bl/6J mice. This strain shows reduced blood pressure response to salt, unlike SJL/J mice, suggesting impaired renal dopamine signaling.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Molecular Biology
Background:
- C57Bl/6J mice are a common model for genetic studies but exhibit salt sensitivity and renal injury resistance.
- Renal dopaminergic function plays a role in regulating blood pressure and sodium balance.
Purpose of the Study:
- To investigate the hypothesis that renal dopaminergic function is defective in C57Bl/6J mice.
- To compare salt sensitivity and renal responses between C57Bl/6J and SJL/J mouse strains.
Main Methods:
- Comparative analysis of blood pressure, urinary dopamine, and sodium excretion under normal and high salt diets in C57Bl/6J and SJL/J mice.
- Measurement of renal receptor expression (D(1)-like, AT(1)) and GRK4.
- Assessment of oxidative stress markers (8-isoprostane) and renal injury.
- Pharmacological manipulation of D(1)-like receptors and parathyroid hormone effects on sodium excretion.
Main Results:
- High salt increased blood pressure in C57Bl/6J but not SJL/J mice, with lower urinary dopamine excretion in C57Bl/6J.
- C57Bl/6J mice exhibited impaired natriuresis and a rightward shift in the blood pressure-natriuresis plot.
- D(1)-like receptor agonist/antagonist treatments affected sodium excretion in SJL/J but not C57Bl/6J mice, indicating defective receptor function in the latter.
- C57Bl/6J mice showed less salt-induced renal injury and oxidative stress compared to SJL/J mice.
Conclusions:
- Defective D(1)-like receptor function is a primary cause of salt sensitivity in C57Bl/6J mice.
- Reduced renal dopamine production may also contribute to salt sensitivity.
- The relative resistance to renal injury in C57Bl/6J mice might be linked to decreased reactive oxygen species production.
