Aim: 

Cardiovascular diseases, such as hypertension, 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). Vasodilator agents such as doxazosin (a₁-adrenoceptor antagonist) are currently used to improve benign prostatic hyperplasia (BPH) symptoms. Nitric oxide (NO) is another potent vasodilator and moderate glandular ischaemic processes promote vasoconstriction of prostatic vascular bed as consequence of decreased NO synthase activity (Hayek y col.,J. Urol. 162: 1527, 1999). There is no information, however, about the mechanisms involved in the NO-induced vasodilatation in the pig prostatic small arteries. Therefore, the current study investigates mechanisms involved in the relaxation to NO endogenously-released and exogenously-added in prostatic resistance vascular bed.

Methods: 

Deep branches of the prostatic artery with an internal lumen diameter of 275-410 micron were dissected out from the glandular parenchyma and mounted in a myograph for isometric force recordings.

Results: 

In noradrenaline (NA)-contracted rings with blockade of the noradrenergic neurotransmission and muscarinic receptors, electrical field stimulation (EFS, 1-16Hz) and exogenous NO (1mM-1mM), frequency- and concentration-dependently relaxed with a maximal responses of 60.96.8% and 87.13.1%, respectively, of the NA-induced contraction. The inhibitors guanylyl cyclase and the BK_Ca channels potently inhibited the relaxations induced by EFS and NO. However, SK_Ca and K_ATP channel blockers failed to modify these responses.

Conclusion: 

These results suggest that NO-induced vasodilatation in the prostatic resistance arteries is produced via a cGMP-dependent mechanism involving activation of BK_Ca channels.

This work was supported by the Medical Foundation of Mutua Madrileña, Inc. (FMM 2006/09, Spain).