ArticleAdvances in pharmacological sciences2010
Testosterone and cholesterol vasodilation of rat aorta involves L-type calcium channel inhibition.
Article in Advances in pharmacological sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 33 citations in OpenAlex.
- The Plasticizer Dibutyl Phthalate (DBP) Impairs Pregnancy Vascular Health: Insights into Calcium Signaling and Nitric Oxide Involvement.Journal of xenobiotics · 2025Article
- UV-B Filter Octylmethoxycinnamate Alters the Vascular Contractility Patterns in Pregnant Women with Hypothyroidism.Biomedicines · 2021Article
- A high throughput zebrafish chemical screen reveals ALK5 and non-canonical androgen signalling as modulators of the pkd2Scientific reports · 2020Article
- UV-B Filter Octylmethoxycinnamate Induces Vasorelaxation by CaInternational journal of molecular sciences · 2019Article
- Article
- Modulation of neointimal lesion formation by endogenous androgens is independent of vascular androgen receptor.Cardiovascular research · 2014Article
- Non-genomic vasorelaxant effects of 17β-estradiol and progesterone in rat aorta are mediated by L-type Ca2+ current inhibition.Acta pharmacologica Sinica · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Testosterone has rapid nongenomic vasodilator effects which could be involved in protective cardiovascular actions. Several authors suggested specific mechanisms to explain this effect, but this matter was not clarified yet. We studied the actions of testosterone and cholesterol on endothelium-denuded rat aorta and their effects on the L-type Ca(2+) current (I(Ca,L)) and potassium current (I(K)). Testosterone (1-100 μM) totally relaxed, in a rapid and concentration-dependent way, the aortic rings contracted by KCl or by (-)-Bay K8644 (BAY). Cholesterol also fully relaxed the contractions induced by KCl. None of the potassium channel antagonists tested (glibenclamide, tetraethylammonium and 4-aminopyridine) modified significantly the relaxant effect of testosterone. The antagonist of classic testosterone receptors, flutamide, did not modify the vasorelaxant effect of testosterone. Furthermore, testosterone and cholesterol inhibited either basal and BAY-stimulated I(Ca,L) in A7r5 cells and they have no effects on I(K). In summary, our results demonstrate that cholesterol and testosterone relax rat aorta by inhibiting LTCC. This effect of testosterone is not mediated by the classic hormone receptor or by potassium channel activation. These results suggest that the vasodilator mechanism of cholesterol and testosterone is the same.
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Registered trials
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