Renal hemodynamic response to ureteral obstruction during converting enzyme inhibition

Urol Res. 1996;24(4):217-27. doi: 10.1007/BF00295895.

Abstract

Acute unilateral obstruction (UUO) of the pig kidney is associated with an increased secretion of intrarenally generated angiotensin II (ANG II). In order to clarify the importance of this intrarenal ANG II generation during acute UUO, ipsilateral and contralateral renal blood flow and renal secretion rate of ANG II were determined in pigs during continuous infusion of an angiotensin I converting enzyme (ACE) inhibitor. Pigs were operatively equipped with electromagnetic flow probes and catheters in the renal veins and aorta. Intravenous administration of the ACE inhibitor SQ14225 (captopril), 1 mg/kg per hour, resulted in a significant increase in renal blood flow in the contralateral kidney from 340 +/- 28 ml/min to 435 +/- 36 ml/min (P < 0.01), whereas renal blood flow in the ipsilateral kidney was significantly reduced from 388 +/- 23 ml/min to 248 +/- 24 ml/min, similar to the reduction in controls. Captopril reduced mean aortic blood pressure, renal vascular resistance consistently on both sides, and plasma concentrations of ANG II and aldosterone from all sample sites. Renal secretion rate of ANG II showed a clear tendency to be reduced from the ipsilateral kidney. The results suggest that in UUO a compensatory increase in renal blood flow may be inhibited in part due to an enhanced secretion of ANG II in the ipsilateral kidney. However, a captopril-mediated inhibition of bradykinin breakdown may also explain some of the observed changes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aldosterone / blood
  • Angiotensin II / blood
  • Angiotensin II / metabolism
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Animals
  • Captopril / pharmacology*
  • Female
  • Hemodynamics / drug effects
  • Kidney / metabolism
  • Pelvis / physiopathology
  • Pressure
  • Renal Circulation / drug effects*
  • Swine
  • Ureteral Obstruction / metabolism
  • Ureteral Obstruction / physiopathology*
  • Vascular Resistance / drug effects
  • Vasopressins / blood

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Vasopressins
  • Angiotensin II
  • Aldosterone
  • Captopril