Pierucci A, Simonetti B M, Ciabattoni G, Taggi F, Morabito S, Vastano S, Pugliese F
Eur J Clin Invest. 1986 Jun;16(3):233-8. doi: 10.1111/j.1365-2362.1986.tb01334.x.
The aim of this research was to study exogenous prostacyclin effect on urinary kallikrein excretion (UKK) in man, to define whether prostacyclin-induced renin release and/or endogenously released cyclooxygenase products were responsible for prostacyclin-induced enhancement of UKK, to determine furosemide effect on UKK. Prostacyclin was infused in eight healthy men and repeated after propranolol and indomethacin treatment. Prostacyclin caused a dose-dependent increase of UKK. Pretreatment with propranolol and indomethacin did not affect prostacyclin-induced enhancement of UKK, although it reduced absolute values of plasma renin activity. Furosemide increased UKK and simultaneously urinary 6-keto-prostaglandin F1 alpha. We conclude that prostacyclin induces an increase in UKK in a dose-dependent manner; furosemide-induced renal prostacyclin synthesis is temporally related to enhancement of UKK; partial dissociation of UKK from plasma renin activity under propranolol and indomethacin treatment and in response to furosemide might suggest a direct effect of prostacyclin on UKK.
本研究的目的是研究外源性前列环素对人体尿激肽释放酶排泄(UKK)的影响,确定前列环素诱导的肾素释放和/或内源性释放的环氧化酶产物是否是前列环素诱导UKK增加的原因,以及确定呋塞米对UKK的影响。对8名健康男性输注前列环素,并在普萘洛尔和吲哚美辛治疗后重复输注。前列环素导致UKK呈剂量依赖性增加。尽管普萘洛尔和吲哚美辛预处理降低了血浆肾素活性的绝对值,但并未影响前列环素诱导的UKK增加。呋塞米增加了UKK,同时增加了尿6-酮-前列腺素F1α。我们得出结论,前列环素以剂量依赖性方式诱导UKK增加;呋塞米诱导的肾前列环素合成在时间上与UKK增加相关;在普萘洛尔和吲哚美辛治疗以及对呋塞米的反应中,UKK与血浆肾素活性部分解离,这可能表明前列环素对UKK有直接作用。