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Role of postnatal dietary sodium in prenatally programmed hypertension
Tyrus Stewart1, Jeannine Ascani, Randall D Craver
1Louisiana State University Health Sciences Center, 1900 Gravier Street, New Orleans, LA 70112, USA.
Insights
Early life dietary sodium intake significantly impacts hypertension development in offspring from protein-restricted mothers. Low sodium diets in early life can prevent and even reverse hypertension, suggesting a critical developmental window for intervention.
Area of Science:
- Nephrology
- Developmental Biology
- Nutritional Science
Background:
- Prenatal programming via maternal low protein (LP) diet induces hypertension in rat offspring.
- Hypertension development is influenced by early life dietary factors, including sodium (Na) intake.
- Oxidative stress, measured by kidney nitrotyrosine content, is implicated in hypertension pathogenesis.
Purpose of the Study:
- To investigate the short- and long-term effects of early life dietary sodium on prenatally programmed hypertension.
- To determine if early dietary sodium exposure can "reprogram" hypertension development.
- To assess the role of salt-induced renal oxidative stress in this hypertension model.
Main Methods:
- Rat offspring from mothers on low protein (LP) or control diets were weaned onto high (HS), standard (SS), or low (LS) sodium diets.
- Blood pressure and kidney oxidative stress markers were assessed.
- A subset of LP offspring received brief early postnatal exposure to HS or LS diets, followed by SS diet, and were monitored long-term.
Main Results:
- LP offspring on SS diet developed hypertension by 6 weeks; LS diet prevented it, HS diet exacerbated it.
- LS diet reduced kidney nitrotyrosine content compared to HS diet in LP offspring.
- Early 3-week exposure to LS diet in LP offspring prevented later hypertension, reduced nephrosclerosis, and abolished salt-sensitivity.
Conclusions:
- Hypertension in this model is salt-sensitive and may involve salt-induced renal oxidative stress.
- Early postnatal dietary sodium manipulation can "reprogram" the trajectory of programmed hypertension.
- A critical developmental window exists for mitigating the long-term effects of prenatal programming on hypertension.
Abstract:
In this study we examined the short- and long-term impact of early life dietary sodium (Na) on prenatally programmed hypertension. Hypertension was induced in rat offspring by a maternal low protein (LP) diet. Control and LP offspring were randomized to a high (HS), standard (SS), or low (LS) Na diet after weaning. On the SS diet, the LP pups developed hypertension by 6 weeks of age. The development of hypertension was prevented by the LS diet and exacerbated by the HS diet. Kidney nitrotyrosine content, a measure of oxidative stress, was reduced by the LS diet compared with the HS diet. The modified diets had no effect on control pups. A group of animals on the SS diet was followed up to 51 weeks of age after an early life 3-week exposure to the HS or LS diet. This brief early exposure of LP animals to the LS diet prevented the later development of hypertension and ameliorated the nephrosclerosis observed after early exposure to the HS diet. The LP offspring with early exposure to LS diet had lost their salt-sensitivity when challenged with the HS diet at the age of 43-49 weeks. No effect of early life dietary Na was observed in control animals. These results show that hypertension in this model is salt sensitive and may, in part, be mediated by salt-induced renal oxidative stress and that there may exist a developmental window which allows postnatal "reprogramming" of the hypertension.
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