Changes in Blood Pressure and Abundance of Kidney Sodium Channels in Postpartum Preeclamptic Rats




McCafferty, Adair
Smith, Jonna
Smith, Savanna
Jones, Kylie
Castillo, Angie
Wiemann, Natalia
Owen, Malissa
Srivastava, Riti
Cunningham, Mark


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Purpose: Postpartum (PP) preeclamptic (PE) women have an increased risk of developing hypertension (HTN) and chronic kidney disease. However, the mechanisms of these diseases in PP PE women are not fully understood. Results from our previous studies show 10-week PP PE rats have HTN (PMID: 34727994). One factor that could cause elevated blood pressure is an increase in sodium transport in the kidneys of PP PE rats. Our current study will examine the BP as well as the amount of Sodium Potassium Chloride Cotransporters (NKCC), Sodium Hydrogen Exchanger-1 (NHE1) and a-subunit of the Epithelial Sodium Channel (ENaC) within the kidney of PE rats 6 weeks postpartum (PP6). We hypothesize that PP6 PE rats will have an increase in BP as well as increased amounts of NKCC, NHE1 and a-ENaC proteins.

Methods: Pregnant Sprague Dawley rats were divided into 2 group: control (CON) normal pregnant rats and PE rats (derived from the surgically induced placental ischemic model of PE). All rats gave birth and were weaned for 3 weeks. At PP6, BP was measured via carotid catheterization. Kidney cortex (KC) and medulla (KM) tissue were collected to measure for NKCC, NHE1 and a-ENaC amounts via Western Blots.

Results: BP was significantly elevated in PP6 vs CON rats (128 ± 6 vs 106 ± 4mmHg, p<0.05). The amount of NKCC channels within the KC was significantly increased in PP6 vs CON rats (107.82 ± 5.64 vs 100 ± 1.48 IU/Protein/CON%, p<0.05). The amount of a-ENaC proteins within the KC was also increased in PP6 vs CON rats (123.4 ± 4.67 vs 116.5 ± 33.03 IU/Protein/CON%, p=0.06). NHE1 channels within the KC were slightly decreased in PP6 vs CON rats (77.31 ± 15.28 vs 100 ± 16.61 IU/Protein/CON%, N.s). No changes were observed in a-ENaC proteins within the KM in PP6 vs CON rats.

Conclusion: PP6 PE rats have HTN as well as increased NKCC and a-ENaC sodium transport proteins in the kidney cortex. These results confirm our hypothesis that increased sodium transporters in the kidney, which could elevate sodium and water reabsorption, correlates with an increase in blood pressure. This study is clinically relevant because it informs clinicians on the pathophysiology of HTN and renal disease/dysfunction in PP PE women. It also highlights novel approaches to providing potential therapies to manage blood pressure in PP PE women. Future studies will investigate the cause-and-effect relationship between blood pressure and sodium handling in the kidney of PP PE rats.