Mechanisms involved in testosterone-induced vasodilatation in pig prostatic small arteries

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.

The testosterone vasoactive effects were assessed in small arterial rings mounted in microvascular myographs for isometric force recordings.

Testosterone and the non-aromatizable metabolite 4, 5alpha-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), 5alpha-reductase, prostanoid synthesis and K(+) channels, failed to modify the responses to testosterone. In Ca(2+)-free 124 mM KPSS, testosterone markedly inhibited in a concentration-dependent manner the contraction curve t degrees CaCl(2). In arteries pretreated with an L-type voltage-activated Ca(2+) channels (VOCCs) inhibitor, nifedipine, testosterone still relaxed noradrenaline-precontracted arteries.

These data suggest that testosterone induces a direct vasodilatory action in pig prostatic small arteries independent of either endothelium, NO, prostanoids, aromatase or 5alpha-reductase activities, AR or K(+) channels. Such an effect is suggested to be produced via blockade of extracellular Ca(2+) entry through L-type VOCCs and non-L-type Ca(2+) channels. Testosterone-induced vasodilatation could be useful to prevent prostatic ischemia.