Prostaglandin type E activity dominates in urinary tract smooth muscle in vitro.
Changes in isometric tension and spontaneous contractions in human and porcine lower urinary tract smooth muscle strips caused by PGE2, PGF2a and the prostaglandin biosynthesis inhibitor ketoprofen were investigated in vitro. Ketoprofen reduced the prostaglandin 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. PGF2a increased the tension in all strips. The threshold concentration for prostaglandin effect in strips pretreated with ketoprofen was 10(-10) - 10(-9) mol./l., a concentration which might be considered physiologically relevant. Prostaglandin synthesis inhibition thus caused responses opposite to those of PGE2 in every single strip. These results strongly suggest the PGE-type of activity to be more important than the PGF-type of activity in lower urinary tract smooth muscle in vitro.
D000818:Animals; D015237:Dinoprost; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007660:Ketoprofen / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology*; D011460:Prostaglandins F / Q000502:physiology; D013552:Swine; D014521:Urethra / Q000502:physiology*; D001743:Urinary Bladder / Q000502:physiology*
D011458:Prostaglandins E; D011460:Prostaglandins F; D007660:Ketoprofen; D015237:Dinoprost