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Increased Arterial Responsiveness to Angiotensin II in Mice Conceived by Assisted Reproductive Technologies
Theo Arthur Meister1, Rodrigo Soria1, Afzal Dogar1,2
1Department of Cardiology and Biomedical Research, Inselspital Bern University Hospital, 3010 Bern, Switzerland.
International Journal of Molecular Sciences
|November 11, 2022
Summary
Assisted Reproductive Technologies (ART) may epigenetically alter blood vessel responses to angiotensin II (ANG II). ART offspring show increased arterial responsiveness to ANG II, potentially contributing to hypertension.
Area of Science:
- Cardiovascular Science
- Reproductive Biology
- Epigenetics
Background:
- Assisted Reproductive Technologies (ART) use has increased globally since 1978.
- ART offspring may experience cardiovascular issues like hypertension and vascular dysfunction.
- Epigenetic changes in the renin-angiotensin system are potential mechanisms for ART-induced cardiovascular effects.
Purpose of the Study:
- To investigate if ART increases arterial responsiveness to angiotensin II (ANG II) via epigenetic modification of its receptors.
- To examine the expression of ANG II receptors (AT1R and AT2R) and their promoter methylation in ART mice.
Main Methods:
- Assessed vasoconstrictor response to ANG II in isolated aortas from ART and control mice.
- Quantified ANG II receptor type 1 and type 2 protein expression.
- Analyzed promoter methylation of *At1aR*, *At1bR*, and *At2R* genes.
Main Results:
- ART mice exhibited significantly increased vasoconstrictor response to ANG II compared to controls.
- An elevated AT1R to AT2R protein expression ratio was observed in ART mouse aortas.
- Hypomethylation in the *At1bR* gene promoter correlated with increased gene transcription and AT1R expression.
Conclusions:
- ART epigenetically alters aortic ANG II receptor expression, creating an imbalance favoring vasoconstriction (AT1R) over vasodilation (AT2R).
- This receptor imbalance is a novel mechanism contributing to ART-associated arterial hypertension in mice.
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