Exposure of the Gestating Mother to Sympathetic Stress Modifies the Cardiovascular Function of the Progeny in Male Rats

Beatriz Piquer, Diandra Olmos, Andrea Flores, Rafael Barra, Gabriela Bahamondes, Guillermo Diaz-Araya and Hernan E. Lara ()
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Beatriz Piquer: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile
Diandra Olmos: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile
Andrea Flores: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile
Rafael Barra: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile
Gabriela Bahamondes: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile
Guillermo Diaz-Araya: Department of Chemical Pharmacology and Toxicology, Faculty of Chemistry and Pharmaceutical Sciences, Universidad de Chile, Santiago 8380492, Chile
Hernan E. Lara: Centre for Neurobiochemical Studies in Neuroendocrine Diseases, Laboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Universidad de Chile, Santiago 8380492, Chile

IJERPH, 2023, vol. 20, issue 5, 1-15

Abstract: Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function and sensitivity to in vivo adrenergic stimulation were studied in male progeny. Methods: Pregnant Sprague–Dawley rats were exposed to cold stress (4 °C/3 h/day); rats’ male progeny were euthanized at 20 and 60 days old, and their hearts were used to determine the β-adrenergic receptor (βAR) (radioligand binding) and NE concentration. The in vivo arterial pressure response to isoproterenol (ISO, 1 mg/kg weight/day/10 days) was monitored in real time (microchip in the descending aorta). Results: Stressed male progeny presented no differences in ventricular weight, the cardiac NE was lower, and high corticosterone plasma levels were recorded at 20 and 60 days old. The relative abundance of β1 adrenergic receptors decreased by 36% and 45%, respectively ( p < 0.01), determined by Western blot analysis without changes in β2 adrenergic receptors. A decrease in the ratio between β1/β2 receptors was found. Displacement of 3 H-dihydroalprenolol (DHA) from a membrane fraction with propranolol (β antagonist), atenolol (β1 antagonist), or zinterol (β2 agonist) shows decreased affinity but no changes in the β-adrenergic receptor number. In vivo exposure to ISO to induce a β-adrenergic overload provoked death in 50% of stressed males by day 3 of ISO treatment. Conclusion: These data suggest permanent changes to the heart’s adrenergic response after rat progeny were stressed in the uterus.

Keywords: gestational programming; cardiovascular; norepinephrine; beta receptors (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2023
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