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Schnermann J, Huang YG, Briggs JP. Angiotensin II blockade causes acute renal failure in eNOS-deficient mice. J Renin Angiotensin Aldosterone Syst. 2001;2(1):S199-S203doi: 10.1177/14703203010020013501.
Schnermann, J., Huang, Y. G., & Briggs, J. P. (2001). Angiotensin II blockade causes acute renal failure in eNOS-deficient mice. Journal of the renin-angiotensin-aldosterone system : JRAAS, 2(1), S199-S203. https://doi.org/10.1177/14703203010020013501
Schnermann, Jürgen, et al. "Angiotensin II blockade causes acute renal failure in eNOS-deficient mice." Journal of the renin-angiotensin-aldosterone system : JRAAS vol. 2,1 (2001): S199-S203. doi: https://doi.org/10.1177/14703203010020013501
Schnermann J, Huang YG, Briggs JP. Angiotensin II blockade causes acute renal failure in eNOS-deficient mice. J Renin Angiotensin Aldosterone Syst. 2001 Mar;2(1):S199-S203. doi: 10.1177/14703203010020013501. PMID: 28095225.
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J Renin Angiotensin Aldosterone Syst. 2001 Mar;2(1):S199-S203. doi: 10.1177/14703203010020013501.

Angiotensin II blockade causes acute renal failure in eNOS-deficient mice.

Journal of the renin-angiotensin-aldosterone system : JRAAS

Jürgen Schnermann, Yuning G Huang, Josie P Briggs

Affiliations

  1. National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA, jurgens@ intra.niddk.nih.gov.
  2. National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.

PMID: 28095225 DOI: 10.1177/14703203010020013501

Abstract

Compared with wild-type mice, adult endothelial nitric oxide synthase (eNOS) knockout mice (eight months of age) have increased blood pressure (BP) (126±9 mmHg vs. 100±4 mmHg), and an increased renal vascular resistance (155±16 vs. 65±4 mmHg.min/ml). Renal vascular resistance responses to i.v. administration of noradrenaline were markedly enhanced in eNOS knockout mice. Glomerular filtration rate (GFR) of anaesthetised eNOS -/- mice was 324±57 µl/min gKW, significantly lower than the GFR of 761±126 µl/min.gKW in wild-type mice. AT1-receptor blockade with i.v. candesartan (1-1.5 mg/kg) reduced arterial blood pressure and renal vascular resistance, and increased renal blood flow (RBF) to about the same extent in wild-type and eNOS -/- mice. Candesartan did not alter GFR in wild-type mice (761±126 vs. 720±95 µl/min.gKW), but caused a marked decrease in GFR in eNOS -/- mice (324.5±75.2 vs. 77±18 µl/min.gKW). A similar reduction in GFR of eNOS deficient mice was also caused by angiotensin-converting enzyme (ACE) inhibition. Afferent arteriolar granularity, a measure of renal renin expression, was found to be reduced in eNOS -/- compared with wild-type mice. In chronically eNOS-deficient mice, angiotensin II (Ang II) is critical for maintaining glomerular filtration pressure and GFR, presumably through its effect on efferent arteriolar tone.

Keywords: candesartan; endothelium; glomerular filtration rate; nitric oxide synthase; quinapril; renal blood flow

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