Prejunctional α-adrenoceptors regulate nitrergic neurotransmission in the rabbit urethra

Abstract We evaluated the effects of prejunctional α-adrenoceptors on nitric oxide (NO)-mediated urethral relaxation in rabbits using a muscle bath technique and high-performance liquid chromatography coupled with a microdialysis procedure. The amount of NO 2 − /NO 3 − released during electrical field stimulation was measured by an NO 2 − /NO 3 − analyzer based on the Griess method. Pretreatment with phenylephrine (0.01 μM) and yohimbine (0.1–10 μM) significantly reduced the relaxation responses induced by electrical field stimulation. In contrast, pretreatment with clonidine (0.01 μM) and prazosin (0.01–1 μM) enhanced the relaxation responses. Cys-NO-induced relaxations of rabbit urethral smooth muscle were not affected by pretreatment with α-adrenoceptor agonists and antagonists. The amount of NO 2 − /NO 3 − released by electrical field stimulation increased after pretreatment with clonidine (0.01 μM) and prazosin (0.01–1 μM), but decreased after pretreatment with phenylephrine (0.01 μM) and yohimbine (0.1–10 μM). The results suggest that the release of NO from nitrergic nerves in the rabbit urethra is reduced and increased by stimulation of prejunctional α 1 - and α 2 -adrenoceptors, respectively.