This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Schnermann, J. Articles by Briggs, J. P Search for Related Content PubMed Articles by Schnermann, J. Articles by Briggs, J. P Social Bookmarking                   What's this?

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

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

Yuning G Huang

National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA

Josie P Briggs

National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA

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.

Key Words: candesartan • quinapril • nitric oxide synthase • glomerular filtration rate • renal blood flow • endothelium

Journal of Renin-Angiotensin-Aldosterone System, Vol. 2, No. 1 suppl, S199-S203 (2001)
DOI: 10.1177/14703203010020013501


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				P. B. Hansen, S. Hashimoto, M. Oppermann, Y. Huang, J. P. Briggs, and J. Schnermann Vasoconstrictor and Vasodilator Effects of Adenosine in the Mouse Kidney due to Preferential Activation of A1 or A2 Adenosine Receptors J. Pharmacol. Exp. Ther., December 1, 2005; 315(3): 1150 - 1157. [Abstract] [Full Text] [PDF]