Toxicological sciences : an official journal of the Society of ToxicologyNov 13, 2013

Higher blood pressure in rat offspring after mothers are exposed to various chemicals during pregnancy

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 2, 2026

Abstract

Male offspring exposed to dexamethasone, perfluorooctane sulfonate, atrazine, and perfluorononanoic acid exhibited 7-10 weeks of elevated blood pressure.

Exposure to certain toxicants during pregnancy is linked to increased blood pressure in offspring.
Female offspring showed higher blood pressure at 10 weeks for perfluorononanoic acid and arsenic, with continued elevation at 37 weeks for dexamethasone, perfluorooctane sulfonate, and atrazine.
By 52-65 weeks, only offspring from dexamethasone, perfluorooctane sulfonate, and atrazine continued to show elevated blood pressure.
Lower nephron counts were associated with elevated blood pressure in the offspring.
Increased renal gene expression for glucocorticoid receptors was observed in offspring exposed to dexamethasone, perfluorooctane sulfonate, and atrazine.
Maternal exposure to toxicants may induce elevated blood pressure in offspring, potentially linked to maternal stress affecting weight gain.

Simplified

Adverse intrauterine environments have been associated with increased risk of later cardiovascular disease and hypertension. In an animal model using diverse developmental toxicants, we measured blood pressure (BP), renal nephron endowment, renal glucocorticoid receptor (GR) gene expression, and serum aldosterone in offspring of pregnant Sprague Dawley rats exposed to dexamethasone (Dex), perfluorooctane sulfonate (PFOS), atrazine, perfluorononanoic acid (PFNA), arsenic, or nicotine. BP was assessed by tail cuff photoplethysmography, nephron endowment by confocal microscopy, and renal GR mRNA by qPCR. BP was also measured by telemetry, and corticosterone (CORT) was measured in resting or restrained Dex and atrazine offspring. Treated dams gained less weight during treatment in all groups except arsenic. There were chemical- and sex-specific effects on birth weight, but offspring body weights were similar by weaning. BP was higher in Dex, PFOS, atrazine, and PFNA male offspring by 7-10 weeks. Female offspring exhibited elevated BP at 10 weeks for PFNA and arsenic, and at 37 weeks for Dex, PFOS, and atrazine. Dex, PFOS, and atrazine offspring still exhibited elevated BP at 52-65 weeks of age; others did not. Elevated BP was associated with lower nephron counts. Dex, PFOS, and atrazine offspring had elevated renal GR gene expression. Elevations in BP were also observed in Dex and atrazine offspring by radiotelemetry. Atrazine offspring exhibited enhanced CORT response to restraint. Elevated offspring BP was induced by maternal exposure to toxicants. Because all treatments affected maternal gestational weight gain, maternal stress may be a common underlying factor in these observations.

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Higher blood pressure in rat offspring after mothers are exposed to various chemicals during pregnancy

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