Abstract
BackgroundExposure to an adverse environment in early life can have lifelong consequences for risk of cardiovascular disease. Maternal alcohol (ethanol) intake is common and associated with a variety of harmful effects to the fetus. However, examining the effects on the cardiovascular system in adult offspring has largely been neglected. The objectives of this study were to investigate the influence of chronic, low ethanol consumption throughout pregnancy on blood pressure, vascular reactivity and wall stiffness, all key determinants of cardiovascular health, in both male and female rat offspring.MethodsFemale Sprague-Dawley rats were fed an ad libitum liquid diet ± 6% vol/vol ethanol throughout pregnancy. Male and female offspring were studied at 12 months of age. Arterial pressure, heart rate and locomotor activity were measured over 7 days via radiotelemetry. Renal lobar arteries were isolated and studied using wire and pressure myography.ResultsBasal mean arterial pressure in female ethanol-exposed rats was reduced by ~ 5–6 mmHg compared to control female offspring, whereas arterial pressure was unaffected in male offspring. Ethanol-exposed offspring had an attenuated pressor response to an acute restraint stress, with this effect most evident in females. Renal artery function was not affected by prenatal ethanol exposure.ConclusionsWe show for the first time that low level chronic maternal alcohol intake during pregnancy influences arterial pressure in adult offspring in the absence of fetal growth restriction.
Highlights
Exposure to an adverse environment in early life can have lifelong consequences for risk of cardiovascular disease
There were no consistent differences in arterial pressure, heart rate (HR) or locomotor activity over the 24-h period (Fig. 1; all Ptrt > 0.05)
Two-way ANOVA of arterial pressure, HR and locomotor activity revealed an interaction between EtOH exposure and time (Fig 1; all Ptrt*time < 0.01)
Summary
Exposure to an adverse environment in early life can have lifelong consequences for risk of cardiovascular disease. Chronic exposure to ethanol throughout pregnancy (6.36% vol/vol EtOH in liquid diet, E2-birth) led to elevated mean arterial pressure (MAP) and impaired aortic endothelium-dependent relaxation in rat offspring at 25 weeks of age [19]. A similar study in rats (6% vol/vol EtOH in liquid diet, E0 to birth) showed evidence of left ventricular hypertrophy and cardiac fibrosis male and female offspring at 8 months of age [20]. These results indicate that excessive and/or prolonged ethanol exposure during gestation has long-lasting effects on cardiovascular health
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