Enhanced intrarenal angiotensin II generation in response to obstruction of the pig ureter

Am J Physiol. 1992 Sep;263(3 Pt 2):F527-33. doi: 10.1152/ajprenal.1992.263.3.F527.

Abstract

The effect of acute unilateral complete ureteral obstruction (UUO) on renal hemodynamics has been examined in a pig model. Pigs were operated on under general anesthesia, electromagnetic flow probes were inserted around renal arteries, and catheters were implanted in renal veins and aorta for blood sampling. The influence of 15 h of obstruction on the physiological variation in immunoreactive angiotensin II (ANG II) was measured together with detailed analysis of the renal handling of ANG II in anesthetized animals. Pelvic pressure rose significantly within 2 h to a maximum of 59.9 +/- 2.9 cmH2O (n = 10). The ipsilateral renal blood flow (RBF) was reduced by 30% from 319 +/- 35 to 241 +/- 42 ml/min (P = 0.001), whereas contralateral RBF did not change. A temporary significant increase in mean aortic blood pressure was seen during the first 2 h after UUO. Renal vascular resistance increased by 44% in the obstructed kidney from 37 +/- 3 to 55 +/- 9 mmHg.ml-1.min.g during the course of obstruction. Concomitantly, the plasma concentration of immunoreactive ANG II increased from all three sample sites by 8-15 times. This increase was highly significant compared with the sham-operated group. The results show that the pig kidney responds to UUO by a net secretion of ANG II from the ipsilateral kidney. Our observations on the ANG II renal secretion rate suggest that part of the immunoreactive ANG II in the renal venous effluent originated de novo from intrarenal generation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / biosynthesis*
  • Angiotensin II / blood
  • Angiotensin II / metabolism
  • Animals
  • Blood Pressure
  • Central Venous Pressure
  • Female
  • Kidney / metabolism*
  • Pelvis
  • Pressure
  • Renal Circulation
  • Swine
  • Ureteral Obstruction / metabolism*

Substances

  • Angiotensin II