ArticleThe journal of physiological sciences : JPS2017
Arrhythmogenic effect of androgens on the rat heart.
Article in The journal of physiological sciences : JPS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Development and prenatal exposure to androgens alter potassium currents in gonadotropin-releasing hormone neurons from female mice.Journal of neuroendocrinology · 2024Article
- Brugada Syndrome: More than a Monogenic Channelopathy.Biomedicines · 2023Review
- Harnessing the power of nutritional antioxidants against adrenal hormone imbalance-associated oxidative stress.Frontiers in endocrinology · 2023Review
- Asparagine-linked glycosylation modifies voltage-dependent gating properties of CaThe journal of physiological sciences : JPS · 2019Article
- Testosterone-mediated upregulation of delayed rectifier potassium channel in cardiomyocytes causes abbreviation of QT intervals in rats.The journal of physiological sciences : JPS · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In most species androgens shorten the cardiac action potential and reduce the risk of afterdepolarizations. Despite the central role of the rat model in physiological studies, the effects of androgens on the rat heart are still inconclusive. We therefore performed electrophysiological studies on the perfused rat right ventricular free wall. We found a correlation between androgenic activity and a propensity to generate ventricular ectopic action potentials. We also found that the testosterone treatment increased action potential duration at 90 % of repolarization (APD90), while androgenic inhibition increased the time to peak and decreased APD90. We observed that the voltage-gated potassium channel Kv4.3 and the bi-directional membrane ion transporter NCX in the rat myocardium were regulated by androgenic hormones. One possible explanation for these findings is that due to the expression of specific ion channels in the rat myocardium, the action potential response to its hormonal background is different from those described in other experimental models. Our results indicate that androgenic control of NCX expression plays a key role in determining arrhythmogenicity in the rat heart.
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Registered trials
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