Usberti M, Federico S, Di Minno G, Ungaro B, Ardillo G, Pecoraro C, Cianciaruso B, Cerbone A M, Cirillo F, Pannain M
Am J Physiol. 1985 Feb;248(2 Pt 2):F254-9. doi: 10.1152/ajprenal.1985.248.2.F254.
To verify whether angiotensin II (ANG II) stimulates ADH release in humans and to evaluate whether endogenous prostaglandins influence the resulting renal effect of ADH, nonpressor and low pressor doses of ANG II were infused in nine normal volunteers under normal conditions (control study) and after prostaglandin synthesis inhibition with aspirin (ASA study). During ANG II infusion plasma ADH increased in both conditions. Plasma PGE2, urinary PGE2, and urinary 6-keto-PGF1 alpha increased only in the control study, whereas they were undetectable in the plasma and significantly reduced in the urine in the ASA study. ANG II caused a significant fall of glomerular filtration rate, renal plasma flow (with an increase in filtration fraction), fractional sodium excretion, and urine output in both studies. Despite the reduced urine output, urine osmolality decreased significantly in the control study, whereas it increased after aspirin administration. These results suggest that intravenous ANG II stimulates ADH release in humans but that the renal effects of the resulting increase in plasma ADH are different depending on the presence or absence of endogenous prostaglandins.
为了验证血管紧张素II（ANG II）是否刺激人类抗利尿激素（ADH）释放，以及评估内源性前列腺素是否影响ADH产生的肾脏效应，在正常条件下（对照研究）以及在用阿司匹林抑制前列腺素合成后（ASA研究），对9名正常志愿者输注非升压和低升压剂量的ANG II。在输注ANG II期间，两种情况下血浆ADH均升高。血浆PGE2、尿PGE2和尿6-酮-PGF1α仅在对照研究中升高，而在ASA研究中，它们在血浆中无法检测到，且尿中显著降低。在两项研究中，ANG II均导致肾小球滤过率、肾血浆流量（滤过分数增加）、钠排泄分数和尿量显著下降。尽管尿量减少，但在对照研究中尿渗透压显著降低，而在给予阿司匹林后尿渗透压升高。这些结果表明，静脉注射ANG II可刺激人类ADH释放，但血浆ADH升高产生的肾脏效应因内源性前列腺素的存在与否而有所不同。
