Developmental regulation of cardiovascular function is dependent on both genotype and environment

Area of Science:

• Cardiovascular physiology
• Developmental biology
• Genetics

Background:

• Adverse developmental environments can increase adult cardiovascular disease risk.
• Genotype plays a crucial role in individual susceptibility.
• Genetically distinct mouse strains are valuable for dissecting complex traits.

Purpose of the Study:

• To investigate the impact of prenatal nutrient restriction (R) on adult cardiovascular function in A/J (AJ) and C57BL/6J (B6) mice.
• To determine if a postnatal high-fat (HF) diet exacerbates these effects.

Main Methods:

• Pregnant AJ and B6 mice received either a 30% nutrient restriction (R) or ad libitum diet.
• Offspring were fed either a high-fat (HF) or control diet postnatally.
• Cardiovascular parameters including arterial pressure, heart rate, and myocardial performance (Tei index) were assessed at 9 and 25 weeks.

Main Results:

• Prenatal nutrient restriction induced hypertension in B6 mice and abolished normal arterial pressure decline in AJ mice.
• Heart rate changes were strain-dependent following prenatal nutrient restriction.
• The Tei index increased in both AJR and B6R mice, indicating improved global myocardial performance.
• A postnatal high-fat diet did not exacerbate the cardiovascular effects of prenatal nutrient restriction.

Conclusions:

• Prenatal nutrient restriction causes strain-dependent alterations in adult cardiovascular function.
• The genetic background of mice significantly influences their response to developmental nutritional challenges.
• A postnatal high-fat diet does not worsen the cardiovascular outcomes associated with prenatal nutrient restriction in these models.