Kimbrough H M, Vaughan E D, Carey R M, Ayers C R
Circ Res. 1977 Feb;40(2):174-8. doi: 10.1161/01.res.40.2.174.
The effects of intrarenal infusion of 1-sar-8-ala angiotension II (P 113) and a converting enzyme inhibitor, SQ 20881, at doses that did not affect systemic blood pressure (2.0 mug/kg per min) were studied in conscious, uninephrectomized dogs. In dogs receiving approximately equal to 5 mEq/day of sodium, intrarenal infusion of P 113 increased renal blood flow (RBF) from 219.8 +/- 32.3 to 282.7 +/- 20.0 ml/min (P less than 0.004), and with intrarenal SQ 20881 infusion from 215.3 +/- 14.2 to 278.0 +/- 22.2 ml/min (p less than 0.005). In sodium-restricted dogs (approximately equal to 5 mEq/day), glomerular filtration rate (GFR) also increased with intrarenal P 113 infusion from 57.9 +/- 5.7 to 66.3 +/- 6.6 ml/min (P less than 0.05), and with SQ 20881 infusion from 43.1 +/- 2.1 to 55.7 +/- 4.5 ml/min (P less than 0.01). Dogs on approximately equal to 5 mEq/day of sodium showed significant increases in plasma renin activity (PRA) with intrarenal infusion of the peptides, unmasking a negative feedback inhibition of renin release by angiotensin II. No increases in RBF, GFR, or PRA were seen with infusion without inhibitors, or in dogs give P 113 or SQ 20881 while on approximately equal to 80 mEq/day of sodium. In addition, angiotensin II inhibition increased sodium excretion during sodium restriction. These findings suggest that intrarenal angiotensin II is intimately involved in renal responses to sodium restriction which result in conservation of sodium and water.
在清醒的、单侧肾切除的犬中,研究了肾内输注1- Sar - 8 - Ala血管紧张素II(P 113)和一种转化酶抑制剂SQ 20881(剂量为不影响全身血压,2.0微克/千克每分钟)的作用。在接受约5毫当量/天钠摄入的犬中,肾内输注P 113使肾血流量(RBF)从219.8±32.3增加到282.7±20.0毫升/分钟(P<0.004),肾内输注SQ 20881时,RBF从215.3±14.2增加到278.0±22.2毫升/分钟(P<0.005)。在限钠犬(约5毫当量/天)中,肾内输注P 113时肾小球滤过率(GFR)也从57.9±5.7增加到66.3±6.6毫升/分钟(P<0.05),输注SQ 20881时,GFR从43.1±2.1增加到55.7±4.5毫升/分钟(P<0.01)。接受约5毫当量/天钠摄入的犬在肾内输注这些肽时血浆肾素活性(PRA)显著增加,揭示了血管紧张素II对肾素释放的负反馈抑制。在未用抑制剂输注时,或在给予P 113或SQ 20881且钠摄入量约为80毫当量/天的犬中,未观察到RBF、GFR或PRA增加。此外,血管紧张素II抑制在限钠期间增加了钠排泄。这些发现表明,肾内血管紧张素II密切参与了肾脏对限钠的反应,这些反应导致钠和水的潴留。