Renal oxygenation defects in the spontaneously hypertensive rat: role of AT1 receptors.

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Abstract

The spontaneously hypertensive rat (SHR) has oxidative stress and enhanced O2 usage (Q(O2)) relative to tubular sodium transport (TNa). Angiotensin II (Ang II) acting on Type I receptors (AT1-R) causes renal oxidative stress and functional nitric oxide (NO) deficiency that could enhance O2 usage. Therefore, we investigated the hypothesis that AT1-Rs mediate the inefficient renal oxygenation in the SHR.

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Journal

Journal ID (iso-abbrev): Kidney Int.

Title: Kidney international

ISSN: 0085-2538

ISSN (Print): 0085-2538

Publication date (Electronic): Jan 2003

Volume: 63

Issue: 1

Affiliations

[1 ] Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University, Washington, DC, USA.

Article

Publisher Item ID: S0085-2538(15)48860-X

DOI: 10.1046/j.1523-1755.2003.00729.x

PubMed ID: 12472784

SO-VID: 7b7bf3a2-ac82-47ad-8c02-9a44d0f0a2c1

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