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Developmental sensitivity to high dietary sodium chloride in borderline hypertensive rats
1Department of Psychology, University of Alabama at Birmingham 35294.
Insights
High sodium intake during pregnancy and early life permanently raises blood pressure in susceptible rats. Later high sodium exposure also increases blood pressure, with combined effects.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Nutritional Science
Background:
- Early life nutrition, particularly sodium chloride (NaCl) intake, can influence long-term health outcomes.
- Borderline hypertensive rats serve as a model to study the development of hypertension.
- The impact of high NaCl exposure during critical developmental windows on blood pressure regulation is not fully understood.
Purpose of the Study:
- To investigate the effects of maternal high NaCl diet from conception to weaning versus only during weaning on adult blood pressure in borderline hypertensive rats.
- To determine the impact of subsequent high NaCl diet during adulthood on blood pressure.
- To assess the additive effects of perinatal and adult high NaCl exposure on blood pressure regulation.
Main Methods:
- Borderline hypertensive rats were exposed to high (8%) or normal (1%) NaCl maternal diets from conception to weaning or only during weaning.
- Postweaning rats received either 8% or 1% NaCl diets from 8 to 17 weeks of age.
- Blood pressure, body weight, and autonomic nervous system responses to ganglionic blockade were measured.
Main Results:
- Maternal high NaCl exposure from conception through weaning significantly increased adult blood pressure compared to controls.
- High NaCl exposure solely during the weaning period did not elevate blood pressure.
- Adult high NaCl diet independently increased systolic blood pressure, and its effects were additive to perinatal exposure.
- Perinatal high NaCl exposure led to an increased bradycardic response to ganglionic blockade, indicating altered autonomic regulation.
Conclusions:
- The critical window for high dietary sodium chloride to permanently modulate blood pressure regulation is during prenatal and early postnatal development.
- Early life programming by high sodium intake has lasting effects on cardiovascular control mechanisms.
- Combined perinatal and adult high sodium exposure results in additive increases in blood pressure.
Abstract:
The present study compared the postweaning blood pressures and body weights of borderline hypertensive rats exposed to a high (8%) sodium chloride maternal diet either from conception to weaning or only during the weaning period with borderline hypertensive rats consistently exposed to a normal (1%) sodium chloride maternal diet. Because the effects of early sodium chloride exposure may be most evident during a subsequent challenge, rats from each group were assigned to receive either an 8% sodium chloride or a 1% sodium chloride diet from 8 to 17 weeks of age. Exposure to an 8% sodium chloride diet from conception through weaning increased the adult blood pressure of borderline hypertensive rats compared with that of controls exposed to a 1% sodium chloride diet; exposure to an 8% sodium chloride diet only during weaning did not increase blood pressure. An 8% sodium chloride diet beginning at 8 weeks of age increased systolic blood pressure. The effects of perinatal and adult exposure to high dietary sodium chloride were additive. Behavioral observations and urinary electrolyte measures confirmed that pups exposed to an 8% sodium chloride diet during weaning ingested the high-sodium chloride diet. The blood pressure and heart rate response to autonomic nervous system ganglionic blockade were assessed at 17 weeks of age. Borderline hypertensive rats exposed to an 8% sodium chloride diet from conception through weaning showed an increased bradycardic response, but no difference in depressor response, to ganglionic blockade. These data suggest that the window of developmental sensitivity for modulation of blood pressure regulation by high dietary sodium chloride occurs during prenatal and early postnatal development.