ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: FR-PO323

Increased Renal Protein Expressions of SLC4A4 and SLC4A5 in Salt-Sensitive C57Bl/6J Mice

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Wang, Xiaoyan, George Washington University School of Medicine, Washington, District of Columbia, United States
  • Ma, Xiaobo, George Washington University School of Medicine, Washington, District of Columbia, United States
  • Asico, Laureano D., George Washington University School of Medicine, Washington, District of Columbia, United States
  • Jose, Pedro A., George Washington University School of Medicine, Washington, District of Columbia, United States

Group or Team Name

  • Hypertension & Renal Diseases
Background

C57Bl/6J mice are salt-sensitive caused, in part, by the dysfunction of the renal dopamine D1 receptor. However, the role of renal ion transporters in salt-sensitive mice is not well understood.

Methods

Therefore, we studied the effect of varying amounts of sodium intake on the blood pressure (BP) and renal expression of exchanger/transporters/channels for sodium and other ions in salt-sensitive C57Bl/6J mice and salt-resistant BALB/c mice.

Results

We found that 4% NaCl diet given for 1 wk increased the BP (ΔBP=+20 mm Hg) of C57Bl/6J (male, 3 months old, n=5) but not of sex-and age-matched BALB/c mice (n=5). C57Bl/6J mice on high NaCl intake (1.6%, 4%, 6%) had higher BP (ΔBP=+20 mm Hg) relative to when they were on low or normal NaCl intake (<0.09%, 0.6%, 0.8%). The dietary salt-induced increase in BP was observed in anesthetized and conscious, unanesthetized mice, measured by telemetry. There were no differences in water/food intake, urinary excretion, and serum concentrations of Na+, K+, and Cl- between the two mouse strains. However, high salt intake (4%NaCl) increased the renal protein expressions of SLC4A5 (NBCe2) (162±8% vs. 100±5%) and SLC4A4 (NBC1) (163±12%) compared with normal salt diet in C57Bl/6J mice, which was not observed in BALB/c mice. By contrast, the 4% NaCl diet increased renal SLC26A6 (Pendrin L1) in both C57Bl/6J (190±1%) and BALB/c (161±8%) mice. Increased NaCl intake did not affect the renal protein expression of NHE3 in either mouse strain. Renal protein expressions of NCC and αENaC, but not of NKCC2 and γENaC, were decreased by high salt diet in BALB/c, but not in C57Bl/6J mice.

Conclusion

We conclude that the salt sensitivity of BP in C57Bl/6J mice is associated with increased renal protein expressions of SLC4A4 and SLC4A5 and impaired salt-mediated down-regulation of NCC and αENaC.

Funding

  • NIDDK Support