Effects of acetylcholine, noradrenaline, and prostaglandins on the isolated, perfused human fetal urethra

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Abstract
Preparations of the isolated bladder-urethral junction obtained from human fetuses at midgestation were suspended in Krebs solution (37.degree. C), and the urethral lumen was perfused at a low rate (2 ml/h). Resistance to flow and changes in longitudinal tension were recorded. In additional experiments isometric tension changes were recorded in isolated detrusor strips. The occurrence of adrenergic nerve terminals was investigated by the fluorescence technique of Falck and Hillarp. Acetylcholine (0.1-1.0 .mu.g/ml) produced a concentration-related increase in longitudinal tension and in resistance to flow. The effects were unaffected by phenoxybenzamine (0.1 .mu.g/ml) but were completely inhibited by atropine (0.1 .mu.g/ml). The effect on tension was more marked than that on resitance to flow. Noradrenaline [norepinephrine] (0.005-1.0 .mu.g/ml) produced a concentration related increase in longitudinal tension and in resistance to flow; the effects were abolished by phenoxybenzamine (0.1 .mu.g/ml). The amine had a more pronounced effect on resistance to flow than on longitudinal tension. Prostaglandin F2.alpha. (0.1-0.5 .mu.g/ml) increased longitudinal tension and resistance to flow; the effects were not antagonized by atropine (0.1 .mu.g/ml) or by phenoxybenzamine (0.1 .mu.g/ml). In preparations contracted by noradrenaline or acetylcholine, prostaglandins E1 and E2 (0.02-0.2 .mu.g/ml) decreased resistance to flow and longitudinal tension. Acetylcholine (0.02-0.2 .mu.g/ml) and prostaglandin F2.alpha. (0.0-0.5 .mu.g/ml) contracted, noradrenaline (0.05-0.5 .mu.g/ml) relaxed, and prostaglandin E1 and E2 (0.1-5.0 .mu.g/ml) had no consistent effects on the detrusor strips. Histochemically, no adrenergic nerve terminals could be demonstrated in the detrusor, bladder neck or urethra.