前列腺素E2存在於人類輸尿管中，這可能暗示前列素E2可能與輸尿管之間有某些關係。我們收集人類輸尿管做前列腺素E2的離體實驗，從泌尿手術病患身上取得的輸尿管，放在泰羅（Tyrode’s）溶液中，在攝氏37度以1公克張力懸掛，直到輸尿管穩定。在分別加入前列腺素E2，KG1等溶液以引起輸尿管的等長收縮。研究結果顯示：在indomethacin的濃度足夠抑制前列腺素E2代謝脢的情況下，前列腺素E2仍能幫助輸尿管重新再收縮。而這種收縮並無法被特抓毒素（tetrodotoxin）所抑制，但是可被尼費地平（nifedipine）所抑制。人類輸尿管畐前列腺素E2引起的收縮可能是經由肌膜上鈣離子管道的打開而引起，而非由神經性的傳導所致。

The presence of prostaglandin E2(PGE2) in the human ureter implies that PGE2 has a regulatory role in the ureter. Human ureter specimens were thus collected to study the in vitro effect of PGE2. Ureteral preparations, resected from patients who had received surgery for urological diseases, were placed in warmed Tyrode’s solution (37°C) after a resting tension of 1 gram; a solution of PGE2 or KC1 was added to induce ureteral contraction, isometrically. The PGE2 can help the ureter to resume contractility in the presence of indomethacin at a concentration sufficient to block cyclooxygenase. Tetrodotoxin did not inhibit ureteral contractions induced by PGE2, but the ureteral contraction was abolished by nifedipine. Contraction induced by PGE2 in the human ureter are probably mediated by an opening of the calcium channel in the myogenic membrane, and not via neurogenic stimulation.