Role of EP2 and EP3 PGE2 receptors in control of murine renal hemodynamics

1  Department of Medicine, Duke University and Durham Veterans Affairs Medical Center, Durham 27710; and 2  Departments of Medicine and 3  Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina 27599-7545 The kidney plays a central role in long-term regulation of ar...

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Published in:American journal of physiology. Heart and circulatory physiology 2001-01, Vol.280 (1), p.H327
Main Authors: Audoly, Laurent P, Ruan, Xiaoping, Wagner, Victoria A, Goulet, Jennifer L, Tilley, Stephen L, Koller, Beverly H, Coffman, Thomas M, Arendshorst, William J
Format: Article
Language:English
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Summary:1  Department of Medicine, Duke University and Durham Veterans Affairs Medical Center, Durham 27710; and 2  Departments of Medicine and 3  Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina 27599-7545 The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE 2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE 2 . Specifically, we determined the extent to which the EP 2 and EP 3 receptor subtypes mediate the actions of PGE 2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP 2 or EP 3 ( / ) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP 2 receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP 2 / mice [RBF EP 2 / : 5.3 ± 0.8 ml · min 1 · 100 g kidney wt 1 ; renal vascular resistance (RVR) 19.7 ± 3.6 mmHg · ml 1 · min · g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 ± 0.5 ml · min 1 · 100 g kidney wt 1 ; RVR +/+ : 25.4 ± 4.9 mmHg · ml 1 · min · 100 g kidney wt 1 ). This was also the case for the peak RBF increase after local PGE 2 (500 ng) injection into the renal artery (EP 2 / : 116 ± 4   vs. +/+: 112 ± 2% baseline RBF). In contrast, we found that the absence of EP 3 receptors in EP 3 / mice caused a significant increase (43%) in basal RBF (7.9 ± 0.8 ml · min 1 · g kidney wt 1 , P  
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2001.280.1.h327