PGI2 may play a role in the pathophysiology of dysmenorrhea.
Small longitudinally or helically cut strips from the ascending branch of the uterine artery were mounted in organ chambers for isometric recording of contractile activity. PGI2(3-300 ng/ml) caused a concentration-dependent relaxation of spontaneously active preparations, whereas no inhibitory effect could be observed on non-active strips. Furthermore, the compound counteracted the stimulatory effects of PGE2, PGF2 alpha, and NA, but not that of transmural nerve stimulation. The effect of PGI2 could be of interest in that the compound may balance the action of vasoconstricting agents. A disturbance of this balance may be a hitherto unrecognized contributing pathophysiological mechanism in the development of dysmenorrhea.
D001158:Arteries; D015237:Dinoprost; D015232:Dinoprostone; D004412:Dysmenorrhea / Q000503:physiopathology*; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D014599:Uterus / Q000098:blood supply*
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015237:Dinoprost; D011464:Epoprostenol; D015232:Dinoprostone; D009638:Norepinephrine