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Regulation of oxygen utilization by angiotensin II in chronic kidney disease

Aihua Deng1, Tong Tang, Prabhleen Singh

  • 1Division of Nephrology-Hypertension, Department of Medicine, School of Medicine, University of California, San Diego, San Diego, California 92161, USA. adeng@ucsd.edu

Kidney International
|September 27, 2008
PubMed

Insights

Combined angiotensin II blockade in rats with chronic kidney disease normalized renal oxygen consumption relative to sodium reabsorption. This suggests specific metabolic benefits beyond improved hemodynamics for kidney disease progression.

Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Renal Physiology

Background:

  • Chronic kidney disease (CKD) progression is linked to intrarenal hemodynamic changes.
  • The impact of angiotensin II blockade on metabolic adaptations in CKD remains unclear.
  • Renal oxygen consumption (QO(2)) and its relationship with sodium reabsorption (QO(2)/TNa) are critical indicators of kidney function.

Purpose of the Study:

  • To investigate the effects of combined angiotensin II blockade on renal oxygen consumption and related metabolic factors in a rat model of CKD.
  • To determine if angiotensin II blockade specifically influences QO(2)/TNa independent of hemodynamic changes.

Main Methods:

  • Utilized a remnant kidney model of CKD in rats.
  • Administered combined angiotensin II blockade (captopril and losartan).
  • Measured glomerular filtration rate (GFR), renal blood flow (RBF), renal oxygen consumption (QO(2)), sodium reabsorption (TNa), and nitric oxide synthase-1 (NOS-1) expression.

Main Results:

  • Remnant kidneys exhibited proteinuria, reduced GFR, RBF, and NOS-1, with elevated QO(2)/TNa.
  • Combined blockade normalized these parameters, including QO(2)/TNa, despite unchanged QO(2) and increased sodium reabsorption.
  • Other antihypertensive therapies did not normalize QO(2)/TNa, indicating a specific role for angiotensin II.

Conclusions:

  • Combined angiotensin II blockade normalizes renal oxygen consumption relative to sodium reabsorption in experimental CKD.
  • These metabolic improvements occur independently of changes in blood pressure and GFR.
  • Angiotensin II blockade offers benefits in CKD through mechanisms beyond intrarenal hemodynamics, potentially involving enhanced nitric oxide activity.

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