Journal of hypertension · 2026
Low nephron endowment increases susceptibility to salt-induced elevation of blood pressure in mice.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Serrano Herrera Ileana, Byfield Rushelle L, Bateman David A, Li Ling, Hurst Holly, Silberman Jacob, Al-Awqati Qais, D'Agati Vivette D, Lin Fangming, Good Pamela I
Аннотация
OBJECTIVES: Humans born preterm have low nephron endowment and an increased risk for hypertension and chronic kidney disease (CKD) later in life. The risks of these sequelae are augmented by a higher incidence of postnatal kidney injury from ischemic, hypoxic and/or nephrotoxic insults.
METHODS: To test the hypothesis that congenital nephron deficits in the absence of other renal insults are a risk factor for hypertension, and that salt intake modifies this response, we performed continuous ambulatory blood pressure (BP) monitoring before and after high salt diet in a novel mouse model of low nephron endowment (named Ret UB del ).
RESULTS: We discovered that adult Ret UB del mice and controls have similar systolic and diastolic BP. After high salt diet, Ret UB del males and females had a greater rise in systolic BP, and Ret UB del females had a greater rise in diastolic BP than controls. In contrast, Ret UB del males had less of a rise in diastolic BP, revealing possible sex dimorphisms in mice with low nephron endowment. In females, salt loading was accompanied by less suppression of juxtaglomerular renin and a blunted rise in fractional excretion of urinary sodium, although sample stratification reduced the power to detect significant male-female differences. Ret UB del males had more of a CKD phenotype, suggesting that CKD did not contribute to salt-sensitivity.
CONCLUSIONS: This study shows the impact of a modifiable dietary factor on the development of hypertension in mice with low nephron endowment.
METHODS: To test the hypothesis that congenital nephron deficits in the absence of other renal insults are a risk factor for hypertension, and that salt intake modifies this response, we performed continuous ambulatory blood pressure (BP) monitoring before and after high salt diet in a novel mouse model of low nephron endowment (named Ret UB del ).
RESULTS: We discovered that adult Ret UB del mice and controls have similar systolic and diastolic BP. After high salt diet, Ret UB del males and females had a greater rise in systolic BP, and Ret UB del females had a greater rise in diastolic BP than controls. In contrast, Ret UB del males had less of a rise in diastolic BP, revealing possible sex dimorphisms in mice with low nephron endowment. In females, salt loading was accompanied by less suppression of juxtaglomerular renin and a blunted rise in fractional excretion of urinary sodium, although sample stratification reduced the power to detect significant male-female differences. Ret UB del males had more of a CKD phenotype, suggesting that CKD did not contribute to salt-sensitivity.
CONCLUSIONS: This study shows the impact of a modifiable dietary factor on the development of hypertension in mice with low nephron endowment.