Prostaglandin Type E Activity Dominates in Urinary Tract Smooth Muscle in Vitro

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Abstract
Changes in isometric tension and spontaneous contractions in human and porcine lower urinary tract smooth muscle strips caused by PG[prostaglandin]E2, PGF2.alpha. and the PG biosynthesis inhibitor ketoprofen were investigated in vitro. Ketoprofen reduced the PG biosynthesis significantly and caused reversible and dose dependent decreases of tension and spontaneous contractions in detrusor strips, while tension increase was induced in strips from the urethra, bladder neck and trigone. PGE2 reestablished the tension and the spontaneous activity in the detrusor strips and counteracted the tension increase in strips from the urethra, bladder neck and trigone. PGF2.alpha. increased the tension in all strips. The threshold concentration for PG effect in strips pretreated with ketoprofen was 10-10-10-9 M/l, a concentration which might be considered physiologically relevant. PG synthesis inhibition caused responses opposite to those of PGE2 in every single strip. Apparently, the PGE-type of activity is more important than the PGF-type of activity in lower urinary tract smooth muscle in vitro.