1. ¹Surgery Department, Federal University of Ceara, Fortaleza, Ceara, Brazil
2. ²Veterinary College, State University of Ceara, Fortaleza, Ceara, Brazil
3. ³Department of Pharmacology, UNICAMP, Campinas, Brazil

Correspondence: LF Silva, Surgery Department, Federal University of Ceara, Rua Dr Jose Lino 141 apto 1002, Fortaleza, Ceara 60.165-270, Brazil. E-mail: luciofl@secrel.com.br

Received 14 December 2003; Revised 7 September 2004; Accepted 9 September 2004; Published online 28 October 2004.

Abstract

To investigate the pharmacodynamics of phentolamine in human corpus cavernosum (HCC) with special attention to the role of the K⁺ channels. Strips of HCC precontracted with nonadrenergic stimuli and kept in isometric organ bath immersed in a modified Krebs–Henseleit solution enriched with guanethidine and indomethacine were used in order to study the mechanism of the phentolamine-induced relaxation. Phentolamine caused relaxation (50%) in HCC strips precontracted with K⁺ 40 mM. This effect was not blocked by tetrodotoxin (1 M) (54.64.6 vs 48.96.4%) or (atropine (10 M) (52.76.5 vs 58.65.6%). However, this relaxation was significantly attenuated by L-NAME (100 M) (59.75.8 vs 27.87.1%; P<0.05; n=8) and ODQ (100 M) (62.75.1 vs 26.83.9%; P<0.05; n=8). Charybdotoxin and apamin (K_Ca-channel blockers) did not affect the phentolamine relaxations (54.64.6 vs 59.35.2%). Glibenclamide (100 M), an inhibitor of K_ATP-channel, caused a significant inhibition (56.76.3 vs 11.32.3%; P<0.05; n=8) of the phentolamine-induced relaxation. In addition, the association of glibenclamide and L-NAME almost abolished the phentolamine-mediated relaxation (54.65.6 vs 5.71.4%; P<0.05; n=8). The results suggest that phentolamine relaxes HCC by a nonadrenergic–noncholinergic mechanism dependent on nitric oxide synthase activity and activation of K_ATP-channel.