Pre- and postjunctional adreno- and muscarinic receptor functions in the isolated human corpus spongiosum urethrae.

In isolated tissue from the human corpus spongiosum urethrae (CS) the effects of adrenoreceptor and muscarinic receptor active drugs on release of 3H-noradrenaline (NA) from noradrenergic nerves and on isometric tension were investigated. The electrically induced release of 3H was reduced by clonidine (alpha 2-adrenoreceptor agonist), increased by rauwolscine (alpha 2-adrenoreceptor antagonist), and little affected by phenylephrine (alpha 1-adrenoreceptor agonist) and prazosin (alpha 1-adrenoreceptor antagonist). Isoprenaline (beta 1- and beta 2-adrenoreceptor agonist) and procaterol (beta 2-adrenoreceptor agonist) increased the release, propranolol (beta 1- and beta 2-adrenoreceptor antagonist) reduced it, and prenalterol (beta 1-adrenoreceptor agonist) and atenolol (beta 1-adrenoreceptor antagonist) had no effect. Carbachol (muscarinic receptor agonist) decreased and scopolamine (muscarinic receptor antagonist) increased stimulation-induced efflux of 3H. NA, phenylephrine and clonidine contracted isolated CS preparations, clonidine being less potent and having less intrinsic activity than phenylephrine. Prazosin was more effective than rauwolscine for inhibition of NA-induced contractions, and prazosin, but not rauwolscine, abolished electrically induced contractions. Isoprenaline and procaterol, but not prenalterol, relaxed NA-contracted preparations. These relaxations could be blocked by propranolol but not by atenolol. Acetylcholine and carbachol relaxed NA-contracted preparations but had no contractant effect on any of the preparations tested. The results suggest that prejunctionally in the human CS, the alpha-adrenoreceptors are of alpha 2-type and the beta-adrenoreceptors of beta 2-type. Postjunctionally, the main alpha-adrenoreceptor function seems to be of alpha 1-type and the beta-adrenoreceptor function of beta 2-type. Stimulation of muscarinic receptors may inhibit the effects of NA both by decreasing its release from noradrenergic nerves and by counteracting its postjunctional effects.