The effect of prostaglandin synthesis inhibition on motility of the sheep ureter.
To determine the effect of prostaglandin-synthesis inhibition on ureteral motility, isolated rings of sheep ureters were suspended for recording isometric tension in organ baths filled with Krebs-Henseleit solution. The non-steroidal anti-inflammatory drugs (NSAIDs) indomethacin and diclofenac sodium (10(-5) M) inhibited rhythmic ureteral motility by reducing frequency, amplitude and finally stopping contractions. Prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha and thromboxane B2 were determined by radioimmunoassay in the bathing solution before and after addition of NSAIDs. Peak contractile activity at 100 min of suspension was associated with increased concentration of all three prostanoids and 50 min after addition of indomethacin and diclofenac sodium when rhythmic contractions stopped, concentration dropped to low levels. The concentration of prostaglandins released into the organ bath were not quantitatively related to the frequency of contractions and therefore do not seem to affect pacemaker activity within ureteral smooth muscle but rather intercellular recruitment of myo-genically active fibres. These findings indicate that prostaglandins play a role in the motor control of the ureter, and that non-steroidal anti-inflammatory drugs exert an inhibitory action.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis*; D000818:Animals; D004008:Diclofenac / Q000494:pharmacology*; D015237:Dinoprost; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects / Q000378:metabolism; D011460:Prostaglandins F / Q000096:biosynthesis*; D012756:Sheep; D013929:Thromboxane B2 / Q000096:biosynthesis; D014513:Ureter / Q000187:drug effects* / Q000378:metabolism
D011460:Prostaglandins F; D004008:Diclofenac; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D007213:Indomethacin