Oliver J A, Sciacca R R, Le Cren G, Cannon P J
Prostaglandins. 1982 Nov;24(5):641-56. doi: 10.1016/0090-6980(82)90034-x.
To determine whether the renal vascular effect of arginine vasopressin (AVP) is modulated by renal prostaglandins, renal blood flow (RBF) and renal venous plasma prostaglandin E2 (PGE2) were determined during the infusion of AVP in dogs during control conditions and after the administration of the inhibitor of prostaglandin synthesis, indomethacin. During control conditions, intrarenal administration for 10 min of a dose of AVP calculated to increase arterial renal plasma AVP concentration by 75 pg/ml produced a slight renal vasodilation (p less than 0.01) and an increase in renal venous plasma concentration of PGE2. Renal venous PGE2 concentration during control and AVP infusion averaged 33 +/- 7(2) and 52 +/- 12 pg/ml (p less than 0.05), respectively. After administration of indomethacin, the same dose of AVP induced renal vasoconstriction (p less than 0.05) and failed to enhance renal venous PGE2 concentration (9 +/- 1 to 8 +/- 1 pg/ml). Intrarenal administration of 20 ng/kg . min of AVP for 10 min induced a marked renal vasoconstriction (p less than 0.01) and increased renal venous plasma PGE2. Renal venous PGE2 during control and AVP infusion averaged 31 +/- 10 and 121 +/- 31 pg/ml (p less than 0.01), respectively. Administration of the same dose of AVP following indomethacin produced a significantly greater and longer lasting renal vasconstriction (p less than 0.01) and failed to increase renal venous plasma PGE2 (10 +/- 1 to 9 +/- 1 pg/ml). These results indicate that a concentration of AVP comparable to that observed in several pathophysiological conditions induces a slight renal vasodilation which is mediated by renal prostaglandins. The results also indicate that higher doses of AVP induce renal vasoconstriction and that prostaglandin synthesis induced by AVP attenuates the renal vasoconstriction produced by this peptide.
为了确定精氨酸加压素（AVP）的肾血管效应是否受肾前列腺素调节，在对照条件下以及给予前列腺素合成抑制剂吲哚美辛后，对犬输注AVP期间测定了肾血流量（RBF）和肾静脉血浆前列腺素E2（PGE2）。在对照条件下，肾内给予计算可使动脉肾血浆AVP浓度增加75 pg/ml的剂量的AVP 10分钟，可产生轻微的肾血管舒张（p<0.01）并使肾静脉血浆PGE2浓度增加。对照和输注AVP期间肾静脉PGE2浓度平均分别为33±7(2)和52±12 pg/ml（p<0.05）。给予吲哚美辛后，相同剂量的AVP引起肾血管收缩（p<0.05）且未能提高肾静脉PGE2浓度（从9±1至8±1 pg/ml）。肾内给予20 ng/kg·min的AVP 10分钟可引起明显的肾血管收缩（p<0.01）并增加肾静脉血浆PGE2。对照和输注AVP期间肾静脉PGE2平均分别为31±10和121±31 pg/ml（p<0.01）。吲哚美辛给药后给予相同剂量的AVP产生明显更大且更持久的肾血管收缩（p<0.01）且未能增加肾静脉血浆PGE2（从10±1至9±1 pg/ml）。这些结果表明，与在几种病理生理状况下观察到的浓度相当的AVP浓度可引起轻微的肾血管舒张，这是由肾前列腺素介导的。结果还表明，更高剂量的AVP可引起肾血管收缩，且AVP诱导的前列腺素合成可减弱该肽产生的肾血管收缩。
