It is well-established that cardiovascular diseases, such as hypertension and atherosclerosis, in which a reduction in periferic blood flow is present, may represent extrinsic risk factors for benign prostatic hyperplasia (BPH) (Meigs et al., J. Clin Epidemol. 54: 935, 2001). Another fact which supports that changes in the prostatic vascularization favours an increase in the gland mass is the vasoconstriction of the prostatic vascular bed as consequence of low testosterone plasmatic levels (Lekas et al., Urol. Res. 25: 309, 1997; Shabsig et al., Endocrinology 140: 1920, 1999). There is no information, however, about the mechanisms involved in the effects induced by testosterone on the prostatic blood flow. Therefore, the aim of the present study was to investigate the mechanisms involved in the actions produced by testosterone in the prostatic resistance arteries and its influence on glandular vascularization. Rings with an internal lumen diameter of 350-480 micron were mounted in a myograph for isometric force recordings. On noradrenaline (NA)-precontracted samples, testosterone induced concentration-response dependent relaxations. These responses were unchanged by either androgenic receptor or nitric oxide (NO) synthase blockade. Tetraethylammonium, glibenclamide and 4-aminopyridine, blockers of Ca²⁺-activated, ATP-dependent and voltage-activated K⁺ channels, respectively, did not modify the relaxations to testosterone.

These results suggest that testosterone induced an vasodilatatory action in the prostatic resistance arteries through an independent mechanism of androgenic receptor, NO and K⁺ channels activation.

This work was supported by the Medical Foundation of Mutua Madrileña, Inc. (FMM 2006, Spain).