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JHC exPRESS: First Published January 7, 2008. doi:10.1369/jhc.2007.950220
Copyright © Histochemical Society, Inc.

A more recent version of this article appeared on April 1, 2008.
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Articles

Augmented Renal Vascular nNOS and Renin Protein Expression in Angiotensin Type 1 Receptor Null Mice

Sungmi Park 1 and Lisa M. Harrison-Bernard 1*

1 Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana

* To whom correspondence should be addressed. E-mail: lharris{at}lsuhsc.edu.

Submitted on November 16, 2007
Accepted on 18 December 2007


  Abstract
The present study was performed to determine the influence of absence of angiotensin type 1A (AT1A) and/or AT1B receptor feedback regulation of kidney neuronal nitric oxide synthase (nNOS) and renin protein expression. Kidneys were harvested from wild-type (WT), AT1A-/-, AT1B-/-, and AT1A-/-AT1B-/- mice and immunostained for nNOS and renin protein localization. AT1A-/- and AT1A-/-AT1B-/- kidneys demonstrated an increase in the percent of glomeruli with nNOS positive afferent and interlobular arterioles compared to WT mice. Density of vascular nNOS immunostaining was 20-fold higher in kidneys of AT1A-/- and AT1A-/-AT1B-/- compared to WT mice. Density of macula densa nNOS immunostaining was 7-fold higher in AT1A-/-AT1B-/- than WT mice. The percent of glomeruli positive for juxtaglomerular (JG) cell renin was 3-fold higher, while the density of JG cell renin immunostaining was 15-fold higher in kidneys of AT1A-/- and AT1A-/-AT1B-/- compared to WT mice. Kidneys of AT1A-/- and AT1A-/-AT1B-/- displayed recruitment of renin protein expression along afferent and interlobular arterioles. Absence of AT1 receptor signaling resulted in enhanced nNOS protein expression in both microvascular and tubular structures. The enhanced nitric oxide generation may contribute to the reduced renal vascular tone and blood pressure observed with blockade of the renin-angiotensin system.

Key Words: neuronal nitric oxide synthase, juxtaglomerular cell, transgenic mice, renin recruitment, macula densa cells


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