Ylitalo P, Kaukinen S, Nurmi A K, Seppälä E, Pessi T, Vapaatalo H
Prostaglandins. 1985 Jun;29(6):1063-71. doi: 10.1016/0090-6980(85)90229-1.
Iloprost (ZK 36 374), a stable analog of carbaprostacyclin, was infused for 72 h to nine patients with advanced obliterative arterial disease. Iloprost caused a marked vasodilation and a compensatory increase in cardiac output. The glomerular filtration rate increased by 45% and tubular reabsorption of sodium and water were reduced by 80% and 107%, respectively. The urine excretion rate increased by 122%. Tubular handling of potassium and calcium were not influenced by iloprost but magnesium reabsorption was stimulated. The renin-angiotensin system was not activated while serum angiotensin converting enzyme activity was decreased. Kallikrein excretion in urine was increased 4.4-fold but plasma kininogen, a substrate for kallikrein in producing vasoactive kinins, was unaffected by the drug. Plasma levels of 6-keto-PGF1 alpha and TxB2 were decreased and their excretion in urine increased. Plasma catecholamines were not changed by iloprost. Several of the changes persisted for at least the first postinfusion day. The results indicate that iloprost increases urine excretion rate by increasing glomerular blood flow and by inhibiting sodium and water reabsorptions. The kinin-forming system, but not the renin-angiotensin system or plasma catecholamines, may be activated. The decrease in plasma level of prostanoids can be, at least partly, due to their increased excretions in urine.
依洛前列素(ZK 36 374),一种卡前列环素的稳定类似物,对9例晚期闭塞性动脉疾病患者进行了72小时的输注。依洛前列素引起显著的血管舒张和心输出量的代偿性增加。肾小球滤过率增加了45%,钠和水的肾小管重吸收分别减少了80%和107%。尿排泄率增加了122%。依洛前列素对钾和钙的肾小管处理没有影响,但刺激了镁的重吸收。肾素-血管紧张素系统未被激活,而血清血管紧张素转换酶活性降低。尿中激肽释放酶排泄增加4.4倍,但血浆激肽原(激肽释放酶产生血管活性激肽的底物)不受该药物影响。血浆6-酮-前列环素F1α和血栓素B2水平降低,其尿排泄增加。依洛前列素未改变血浆儿茶酚胺水平。其中一些变化至少在输注后的第一天持续存在。结果表明,依洛前列素通过增加肾小球血流量和抑制钠和水的重吸收来增加尿排泄率。激肽形成系统可能被激活,而肾素-血管紧张素系统或血浆儿茶酚胺未被激活。血浆前列腺素水平的降低至少部分是由于其尿排泄增加。