RT Journal Article
T1 Mechanisms involved in testosterone-induced vasodilatation in pig prostatic small arteries
A1 Navarro Dorado, Jorge
A1 Orensanz Muñoz, Luis Miguel
A1 Recio Visedo, María Paz
A1 Bustamante Alarma, Salvador
A1 Benedito Castellote, Sara
A1 Martínez Gómez, Ana Cristina
A1 García Sacristán, Albino
A1 Prieto Ocejo, Dolores
A1 Hernández Rodríguez, Medardo Vicente
AB Aims: Testosterone is beneficial to the cardiovascular system due to its direct coronary vasodilatory action and its circulatory deficiency is associated with coronary artery disease (CAD), which has been proposed as an extrinsic risk factor for benign prostatic hyperplasia (BPH). Therefore, the current study investigated the mechanisms involved in the testosterone-induced vasodilatation in pig prostatic small arteries.Main methods: The testosterone vasoactive effects were assessed in small arterial rings mounted in micro- vascular myographs for isometric force recordings.Key findings: Testosterone and the non-aromatizable metabolite 4, 5α-dihydrotestosterone (DHT) evoked a similar concentration-dependent relaxation on noradrenaline (NA)-precontracted rings. Similar responses were obtained in preparations contracted with 60 mM K+-enriched physiological saline solution. Endothelium mechanical removal or pre-treatment with blockers of nitric oxide (NO) synthase, guanylate cyclase, aromatase activity, intracellular androgenic receptor (AR), 5α-reductase, prostanoid synthesis and K+ channels, failed to modify the responses to testosterone. In Ca2+-free 124 mM KPSS, testosterone markedly inhibited in a concentration-dependent manner the contraction curve t °CaCl2. In arteries pretreated with an L-type voltage-activated Ca2+ channels (VOCCs) inhibitor, nifedipine, testosterone still relaxed noradrenaline- precontracted arteries.Significance: These data suggest that testosterone induces a direct vasodilatory action in pig prostatic small arteries independent of either endothelium, NO, prostanoids, aromatase or 5α-reductase activities, AR or K+ channels. Such an effect is suggested to be produced via blockade of extracellular Ca2+ entry through L-type VOCCs and non-L-type Ca2+ channels. Testosterone-induced vasodilatation could be useful to prevent prostatic ischemia.
SN 0024-3205
YR 2008
FD 2008-10
LK https://hdl.handle.net/20.500.14352/100825
UL https://hdl.handle.net/20.500.14352/100825
LA eng
NO Navarro-Dorado J, Orensanz LM, Recio P, Bustamante S, Benedito S, Martínez AC, et al. Mechanisms involved in testosterone-induced vasodilatation in pig prostatic small arteries. Life Sciences 2008;83:569–73. https://doi.org/10.1016/j.lfs.2008.08.009.
NO Fundación Mutua Madrileña
DS Docta Complutense
RD 25 ago 2024